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Journal of Medical Molecular Biology 2025 Vol.22 Please wait a minute... For Selected: Download Citations EndNote Reference Manager ProCite BibTeX RefWorks Toggle Thumbnails Select P300 Inhibits Intervertebral Disc Degeneration through Nrf2 / HO-1 / NF-κB Signaling in Rat Scoliosis Model #br# ZHAO Xianbin, GUO Shining, BO Wenting Journal of Medical Molecular Biology    2025, 22 (1): 1-7.   DOI: 10.3870/j.issn.1672-8009.2025.01.001 Abstract （136）      PDF （1364KB）（374）       Knowledge map    Save Objective To investigate the effect and potential regulatory mechanism of histoneacetyltransferase P300 on the degeneration of nucleus pulposus cells (NPCs) in the intervertebral discs in the rat scoliosis model. Methods NPCs were cultured and divided into 4 groups: the untreated control group, the interleukin-1β ( IL-1β) -induced degeneration group ( IL-1β group), the IL-1β combined with P300 treatment group (IL-1β + P300 group), and the P300 treatment alone group ( P300 group). Cell proliferation activity was detected using the Cell Counting Kit-8 (CCK-8) assay. The levels of TNF-α and IL-6 were measured using enzyme-linked immunosorbent assay (ELISA). Cell apoptosis was determined using flow cytometry. The expression levels of sex determining region Y-box 9 ( SOX9 )、 collagen type Ⅱ ( COL-Ⅱ ), matrix metalloproteinase-13 (MMP-13), A disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS-5), inhibitor of nuclear factor-kappa B-α ( IκBα), phosphorylated IκBα ( p-IκBα), phosphorylated NF-κB P65 (p-P65), nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) in the cells were analyzed using Western blotting. Additionally, 40 adult specific pathogen-free (SPF) female SD rats were divided into 4 groups: sham surgery group, scoliosis model group, scoliosis model + P300 group, and scoliosis model + P300 + Nrf2-IN-3 group. The scoliosis model was established by removing the upper limbs and tail of the rats through surgery. In the scoliosis model + P300 group, P300 was intravenously injected [15 mg / (kg· d), 30 d] after modeling. In the scoliosis model + P300 + Nrf2-IN-3 group, P300 [15 mg / ( kg· d), 30 d] and the Nrf2 inhibitor Nrf2-IN-3 [23. 5 mg / ( kg · d), 30 d] were intravenously injected after modeling. After 30 days, the nucleus pulposus tissues from the T12-L1 intervertebral discs were collected, and the expression levels of SOX9, COL-Ⅱ , MMP-13, and ADAMTS-5 were determined usingWestern blotting. Results Compared with the control group, the IL-1β group showed decreasedcell viability, increased cell apoptosis, upregulated expression levels of TNF-α, IL-6, MMP-13, ADAMTS-5, p-P65, and p-IκBα, and downregulated expression levels of SOX9, COL-Ⅱ ,IκBα, Nrf2, and HO-1 (all P< 0. 05). Compared with the IL-1β group, the IL-1β + P300 groupshowed increased cell viability, decreased cell apoptosis, decreased expression levels of TNF-α, IL-6, MMP-13, ADAMTS-5, p-P65, and p-IκBα, and increased expression levels of SOX9,COL-Ⅱ , IκBα, Nrf2, and HO-1 ( all P < 0. 05). Compared with the sham surgery group, thescoliosis model group showed decreased expression levels of SOX9 and COL-Ⅱ , and increased expression levels of MMP-13 and ADAMTS-5 ( all P < 0. 05 ). Compared with the scoliosis modelgroup, the scoliosis model + P300 group showed increased expression levels of SOX9 and COL-Ⅱ ,and decreased expression levels of MMP-13 and ADAMTS-5 ( all P < 0. 05). Compared with thescoliosis model + P300 group, the scoliosis model + P300 + Nrf2-IN-3 group showed decreased expression levels of SOX9 and COL-Ⅱ , and increased expression levels of MMP-13 and ADAMTS-5(all P< 0. 05). Conclusion P300 inhibits intervertebral disc degeneration by regulating the Nrf2 /HO-1 / NF-κB signaling pathway in the rat scoliosis model. Related Articles | Metrics Select Hydatid Antigen B Promote RANKL / NF-κB / TAK1-mediated Osteoclastogenesis via Inhibition of TAZ #br# Wuluhan Mahan, XIE Zengru Journal of Medical Molecular Biology    2025, 22 (1): 8-15.   DOI: 10.3870/j.issn.1672-8009.2025.01.002 Abstract （164）      PDF （2352KB）（276）       Knowledge map    Save Objective To investigate the molecular mechanisms of hydatid antigen-B (Hyd-B) in osteoclastogenesis. Methods Cell experiment group-1: Bone marrow mesenchymal stem cells(BMSCs) were divided into 3 groups (Control group, MCSF + RANKL group, MCSF + RANKL + Hyd-B group), cells in the MCSF + RANKL group and MCSF + RANKL + Hyd-B group were induced to differentiate into osteoclasts by using macrophage colony-stimulating factor (MCSF) combined with soluble receptor activator of nuclear factor-κb ligand (RANKL), and then treated with or without Hyd-B respectively. Cell experiment group-2: BMSCs were divided into Ctrl group and Hyd-B treatment group (Treat group), the effect of Hyd-B on the direct interaction between TAZ and TAK1 was determined by co-immunoprecipitation ( co-IP). IP was performed by using antiTAK1 antibody, and TAZ expression level was detected by IB. Cell experiment group-3: BMSCs were divided into 5 groups: Control group, MCSF + RANKL group, MCSF + RANKL + Hyd-B group, MCSF + RANKL + Hyd-B + TAZ-OE group and MCSF + RANKL + Hyd-B + OE-vector group. TAZ overexpression plasmid or vector plasmid was transfected to the BMSCs in the MCSF + RANKL + Hyd-B + TAZ-OE group and MCSF + RANKL + Hyd-B + OE-vector group respectively. qPCR was used to detect the mRNA expression levels of osteoclast differentiation markers of TRAP and Cathepsin K. Western blotting was used to detect the expression levels of nuclear p-P65, cytoplasmic P65, nuclear NFATc1, p-AKT, AKT, p-ERK 1 / 2, ERK 1 / 2, p-TAZ, TAZ and TAK1. Results Compared with those in the Control group, the TRAP and Cathepsin K mRNA expression levels in the MCSF + RANKL and MCSF + RANKL + Hyd-B groups were increased (P <0. 05); the expression levels of p-P65, p-AKT and p-ERK 1 / 2 were increased (P < 0. 05); theexpression levels of p-P65 and NFATc1 in nucleus were increased (P < 0. 05). The expression levels of the above indicators were further increased in the MCSF + RANKL + Hyd-B group when compared with those in the MCSF + RANKL group ( P < 0. 05). Compared with those in the MCSF +RANKL + Hyd-B group, the expression levels of the above indicators in MCSF + RANKL + Hyd-B +TAZ-OE group were all reduced (P < 0. 05). Co-IP results showed that Hyd-B treatment enhancedthe interaction between TAZ and TAK1 ( P < 0. 05). Compared with those in the Ctrl group, thephosphorylated level of cytoplasmic TAZ in Treat group was increased, the expression level of TAZwas reduced (P< 0. 05). Conclusion Hyd-B can promot the RANKL / NF-κB / TAK1-mediated osteoclastogenesis through inhibition of TAZ. Related Articles | Metrics Select Effect of Lupeol on Proliferation, Migration and Invasion of Lung Adenocarcinoma Cells by Targeting CDC25A #br# ZHU Yexin, DENG Liping Journal of Medical Molecular Biology    2025, 22 (1): 16-22.   DOI: 10.3870/j.issn.1672-8009.2025.01.003 Abstract （166）      PDF （6492KB）（69）       Knowledge map    Save Objective To analyze the effect of lupeol on proliferation, migration, invasion of lung adenocarcinoma cells by targeting CDC25A. Methods The targets of lupeol and their correlation with clinical phenotypes of lung adenocarcinoma were analyzed by bioinformatics. A549 and Calu-3 cells were divided into 6 groups: control group, lupeol group, vector group, lupinol + vector group, silence group and lupinol + silence group. The cells activity, migration and invasion were detected. The xenograft models of nude mice with lung adenocarcinoma were constructed to observe the effects of lupeol on volume and weight of xenograft tumors, and expression levels of Ki67 and CDC25A proteins. The relationship between expression level of CDC25A protein and the concentration and time of lupeol treatment was measured. Results Bioinformatic analysis showed thatCDC25A might be one of lupeol targets, and the expression level of CDC25A was closely related tothe progression of lung adenocarcinoma. The survival rates and colony numbers of A549 and Calu-3cells were decreased with the increase of lupeol concentration (P < 0. 05). The number of migrationand invasion lung adenocarcinoma cells in the lupeol group were significantly lower than those in thecontrol group ( P < 0. 05), the volume and weight of xenograft tumors, the expression levels of Ki67 and CDC25A were significantly lower than those in the control group (P < 0. 05). The expression level of CDC25A was significantly decreased with the increase of time and concentration of lupeol treatment (P < 0. 05). The expression level of CDC25A, the cells activities, the number of colonies and migration and invasion cells in the lupinol + vector group, the silence group and the lupinol +silence group were significantly lower than those in the vector group (P < 0. 05). Conclusion Lupeol can inhibit malignancy of lung adenocarcinoma tumor cells by down-regulating CDC25A. Related Articles | Metrics Select Mechanism of Schisantherin B Inhibiting Proliferation of Uterine Corpus Endometrial Carcinoma Cells and Epithelial-mesenchymal Transition by Targeting PTGS1 #br# YE Jing, LI Ping, ZHAO Jinrong, HAN Ci, ZHANG Xin, XU Yuanyuan, SU Huiling Journal of Medical Molecular Biology    2025, 22 (1): 23-28.   DOI: 10.3870/j.issn.1672-8009.2025.01.004 Abstract （123）      PDF （5694KB）（245）       Knowledge map    Save Objective To analyze the mechanism of Schisantherin B inhibiting the proliferationof uterine corpus endometrial carcinoma ( UCEC ) cells and epithelial-mesenchymal transition( EMT ) by targeting prostaglandin-endoperoxide synthase 1 ( PTGS1 ) . Methods The target( PTGS1) of Schisantherin B was predicted by TargetNet. The relationship between the expression ofPTGS1 and the clinicopathological characteristics of UCEC was analyzed by TCGA database. Thecontrol group, Schisantherin B group and sh-PTGS1 group were set up. The survival and colony formation abilities of cells, and the expression levels of EMT associated proteins were detected. Theeffect of PTGS1 on volume and weight of xenograft tumors, and the level of proliferation index(Ki67) were observed. Ishikawa and HEC108 cell lines with stable overexpression of PTGS1 wereconstructed. The effect of Schisantherin B on survival, colony formation abilities, and expressionlevels of EMT proteins of Ishikawa and HEC108 cells with PTGS1 overexpression were detected. Results Compared with those in the control group, the proliferation and numbers of cell colonies, and the expression levels of PTGS1, Vimentin, N-cadherin and Snail in the sh-PTGS1 group and the Schisantherin B group were significantly decreased, the expression level of E-cadherin in the above two groups was significantly increased; the volume and weight of xenograft tumor tissues,and the expression level of Ki67 in the sh-PTGS1 group were significantly decreased ( P < 0. 05). However, the expression level of E-cadherin was significantly decreased in the PTGS1 overexpression group, the expression levels of PTGS1, Vimentin, N-cadherin, Snail, and the cell viabilities, and number of cell colonies of Ishikawa and HEC108 cells were significantly increased when compared with those in the control group (P< 0. 05). In addition, when compared with those in theSchisantherin B group, the expression level of E-cadherin was significantly decreased in the Schisandrin B + PTGS1 overexpression group, while the expression levels of PTGS1, Vimentin,N-cadherin, Snail were significantly increased (P < 0. 05). Conclusion Schisantherin B may inhibit the proliferation and EMT of UCEC cells by down-regulating PTGS1. Related Articles | Metrics Select Jatrorrhizine Inhibit Progression of Osteosarcoma by Downregulation of MAOB #br# LI Xiaowen, ZHAO Jie, JIANG Liqiang, ZHANG Kai, JIA Haidong, ZHANG Cun Journal of Medical Molecular Biology    2025, 22 (1): 29-34.   DOI: 10.3870/j.issn.1672-8009.2025.01.005 Abstract （124）      PDF （7427KB）（39）       Knowledge map    Save Objective To investigate the effect of jatrorrhizine on the development of osteosarcoma and its mechanism. Methods The targets of jatrorrhizine on osteosarcoma were screenedthrough network pharmacology analysis, and GSEA enrichment was used to analyze the relationshipbetween the expression level of monoamine oxidase B (MAOB) and the clinical phenotypes of osteosarcoma. The cell activities of osteosarcoma cells MG63 and U2OS were detected under differentdoses of jatrorrhizine (0, 2, 4, 8, 16 μmol / L), and the optimal jatrorrhizine dose for follow-upfunctional test was selected. CCK-8 method and Transwell assay were used to detect the cell proliferation, migration and invasion of MG63 and U2OS, and Western blotting was applied to detect theprotein expression levels of cell proliferation-associated antigen Ki67, matrix metalloproteinase 2(MMP2) and MMP9. The subcutaneous transplant models of osteosarcoma in nude mice were established, and the weight and volume of tumor tissues of each group were measured, and the expression level of Ki67 was determined by immunohistochemistry. Western blotting was adopted to detect the effect of jatrorrhizine on the expression level of MABO protein in osteosarcoma cells. shRNA was used to interfere with the expression of MAOB, and its effect on the proliferation of osteosarcomacells was analyzed. Results Ten targets of jatrorrhizine on osteosarcoma, including MAOB, waspredicted by network pharmacology analysis. GSEA enrichment analysis showed that MAOB was related to the prognosis (P< 0. 05) and survival (log-rank P < 0. 05) of osteosarcoma. The viabilityof MG63 and U2OS cells decreased with the increase of the drug dose. The dose of 8 μmol / L was chosen for the follow-up functional test as the viability of osteosarcoma cells decreased by about50 % when the dose of jatrorrhizine reached 8 μmol / L. In vitro experiment showed that comparedwith those in the Control group, the cell proliferation rate of jatrorrhizine group was significantly reduced (P < 0. 05), and the number of invasion cells and migrating cells were significantly decreased (P< 0. 05), and the protein levels of Ki67, MMP2 and MMP9 were significantly downregulated (P< 0. 05). In vivo experiment showed that the growth rate of subcutaneous tumors in nudemice of jatrorrhizine group was significantly reduced ( P < 0. 05), and the weight and volume ofsubcutaneous tumors were lowered (P < 0. 05), and the expression level of Ki67 in tumor tissueswas significantly declined (P< 0. 05). Jatrorrhizine inhibited the expression of MAOB in osteosarcoma cells in a time and concentration-dependent manner in vitro (P < 0. 05). Knockdown of MAOBcould significantly inhibit the proliferation of osteosarcoma cells when compared with shNC group(P< 0. 05). Overexpression of MAOB could reverse the inhibitory effect of jatrorrhizine on the proliferation, invasion and migration of osteosarcoma cells (P< 0. 05). Conclusion The expression level of MAOB is related to the prognosis and survival of osteosarcoma. MAOB promotes cell proliferation, invasion and tumor metastasis. Jatrorrhizine inhibits the proliferation, invasion and migrationof osteosarcoma cells by inhibiting the expression of MAOB. Related Articles | Metrics Select Anti-tumor Effect of Tetramethylpyrazine-containing Serum on Liver Cancer HepG2 Cells #br# ZHANG Yifang, DAI Yi Journal of Medical Molecular Biology    2025, 22 (1): 35-40.   DOI: 10.3870/j.issn.1672-8009.2025.01.006 Abstract （146）      PDF （3433KB）（235）       Knowledge map    Save Objective To explore the effect and mechanism of tetramethylpyrazine ( TMP) -containing serum on proliferation, apoptosis and mitochondrial function of liver cancercells. Methods Serum from SD rats treated with 0, 30, 60, 120 mg / kg of TMP was collected andused to treat cells. Colony formation experiment and CCK-8 were employed to test the proliferation of HepG2 cells. Flow cytometry was performed to detect HepG2 cell cycle and apoptosis, mitochondrial membrane potential changes of HepG2 cells were measured by JC-1 through flow cytometry. Western blotting was used to detect the expression levels of PCNA, P27, cleaved caspase-3 (cas-3), Bax, Bcl-2 and Cyt C in HepG2 cells. SOD and MDA levels in HepG2 cells were detected by kits, and 2, 7-dichlorodiacetate (DCFH-DA) was used to determine the production of reactive oxygen species (ROS) in HepG2 cells. Results Compared with that of the control group, the TMP-containing serum of 60 and 120 mg / kg TMP groups significantly reduced the proliferation of HepG2 cells, and blocked cell cycle, moreover, HepG2 cell apoptosis rate was significantly increased and theantioxidant capacity was significantly reduced. Conclusion TMP-containing serum can inhibit theproliferation of liver cancer cells and induce apoptosis of liver cancer cells through a mitochondrialdependent pathway, and stimulate the generation of ROS to reduce the antioxidant capacity of cancer cells, thereby inhibiting the development of liver cancer. Related Articles | Metrics Select Effect of Kaempferol on Inflammatory Response in Rats with Gestational Diabetes Mellitus via Regulation of IL-6 / STAT3 Signaling Pathway #br# GUO Yanling, YANG Ying, JIANG Tiancong Journal of Medical Molecular Biology    2025, 22 (1): 41-47.   DOI: 10.3870/j.issn.1672-8009.2025.01.007 Abstract （184）      PDF （4916KB）（203）       Knowledge map    Save Objective To investigate the effect of kaempferol (Kpf) on inflammatory responsein rats with gestational diabetes mellitus (GDM) by regulation of the interleukin-6 (IL-6) / signaltransducer and activator of transcription 3 (STAT3) signaling pathway. Methods A rat model ofGDM was constructed by the combination of high fat and high sugar diets and intraperitoneal injection of streptozotocin ( STZ). GDM rats were then randomly divided into 5 groups: Model group, Kpf low-, medium-, and high-dose groups, and activator group ( IL-6 / STAT3 pathway activator rIL-6), with 12 rats in each group, another 12 rats without any special treatment as the control. Intraperitoneal injection of the corresponding drug was performed once a day until the 19th day of pregnancy. Roche blood glucose meter was applied to measure fasting blood glucose ( FBG) in rats. The pregnancy outcomes of rats in each group were analyzed. ELISA method was applied to determine the levels of fasting insulin (FINS) in rat serum and interleukin-6, interleukin-1β (IL-6, IL-1β), and tumor necrosis factor-α ( TNF-α) in placental tissues. Hematoxylin-eosin ( HE) staining was applied to observe pathological damage in rat placental tissues. TUNEL staining was applied to detect apoptosis in placental tissues. The expression levels of IL-6 / STAT3 pathway proteinsin placental tissues were detected by Western blotting. Results The values of FBG, FINS, HOMA-IR, fetal mouse weight, the levels of IL-6, IL-1β, TNF-α, the apoptosis rate of placental tissue cells, the expression levels of IL-6, p-STAT3 / STAT3 proteins in the Model group were increased when compared with those in the control group, while the live birth rate and the number ofoffspring were decreased when compared with those in the control group (P < 0. 05). The values ofFBG, FINS, HOMA-IR, fetal mouse mass, the levels of IL-6, IL-1β, TNF-α, the apoptosis rate of placental tissue cells, and the expression levels of IL-6, p-STAT3 / STAT3 proteins in the Kpf low-, medium-, and high-dose groups were decreased when compared with those in the Model group, while the live birth rate and the number of offspring were increased when compared withthose in the Model group (P < 0. 05). The changes of the above indicators in the activator group were reversed when compared to the Kpf high-dose group (P< 0. 05). Conclusion Kpf can alleviate placental inflammation and insulin resistance in GDM rats. Its mechanism may be related to the inhibition of IL-6 / STAT3 signaling pathway. Related Articles | Metrics Select Effect of High Glucose-induced Oxidative Stress and Inflammatory Response on Apoptosis and Extracellular Matrix Metabolic Imbalance in Nucleus Pulposus Cells #br# GUO Xiaoyan, CAO Sheng, WANG Lingling, XU Kun, YANG Jiaqi, YANG Xue, WANG Jing Journal of Medical Molecular Biology    2025, 22 (1): 48-54.   DOI: 10.3870/j.issn.1672-8009.2025.01.008 Abstract （315）      PDF （2204KB）（321）       Knowledge map    Save Objective To investigate the effect of high glucose treatment on apoptosis and extracellular matrix (ECM) metabolism in rat nucleus pulposus cells (NPC) and to preliminarily explorepossible underlying mechanisms. Methods NPC were isolated from lumbar spine tissues of maleWistar rats. NPC were divided into 6 groups: Control group, Glucose-treated groups (treated with 5mmol / L, 15 mmol / L, and 25 mmol / L glucose, respectively), high glucose + NAC group (treated with 25 mmol / L glucose and 3 mmol / L antioxidant NAC), high glucose + PDTC group (treated with 25 mmol / L glucose and 10 μmol / L NF-κB pathway inhibitor PDTC) . Cell viability and apoptosis were detected by cell counting kit-8 and flow cytometry, respectively. Fluorescent probes were used to detect intracellular reactive oxygen species ( ROS) levels. Enzyme-linked immunosorbent assay was used to detect IL-1β, IL-6 and TNF-α levels. Western blotting was used to detect relevant protein expression levels. Results Compared to the cell viability and apoptosis in the control group, no significant change was observed in the 5 mmol / L and 15 mmol / L glucose groups, however, a significant decrease in cell viability and a significant increase in apoptosis were seen in the 25 mmol / L glucosegroup (P< 0. 05). The expression levels of Bcl-2-associated X protein (Bax), Caspase-3, MMP-3,MMP-9, MMP-13, A disintegrin and metalloproteinase with thrombospondin 4 (ADAMTS-4), and ADAMTS-5 were significantly decreased in the glucose + NAC and glucose + PDTC groups when compared with those in the 25 mmol / L glucose group, whereas the expression levels of Bcl-2, collagenⅡ (COLⅡ), and aggrecan were significantly increased (P< 0. 05). The intracellular ROS levelsand supernatant levels of the IL-1β, IL-6, and TNF-α in the glucose + NAC and glucose + PDTCgroups were significantly lower when compared with those in the 25 mmol / L glucose group (P< 0. 05). In addition, the cellular levels of p-P65 / P65 and p-IκBα / IκBα were significantly reduced in the glucose + NAC and glucose + PDTC groups when compared with those in the 25 mmol / L glucosegroup (P< 0. 05). Conclusion High glucose treatment promotes NPC apoptosis and ECM degradation by inducing oxidative stress and inflammatory responses, which involves the activation of ROS / NF-κB signaling pathway. Related Articles | Metrics Select Effect of DJ-1 Protein Expression on Neurotransmitters Levels in Hippocampus of Depression Rats via PI3K / AKT Signaling Pathway #br# LI Xiaoran, CAI Yunfeng, DING Zhaomeng, SUN Xiangsheng, LU Yuchen Journal of Medical Molecular Biology    2025, 22 (1): 55-61.   DOI: 10.3870/j.issn.1672-8009.2025.01.009 Abstract （93）      PDF （4735KB）（361）       Knowledge map    Save Objective To investigate the effect of DJ-1 protein expression on neurotransmitters levels in the hippocampus of depression rats. Methods Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) was used to detect the apoptosis in hippocampus. Enzyme linked immunosorbent assay was used to determine the levels of tumor necrosis factor-α ( TNF-α) and interleukin 6 (IL-6) in serum, and the levels of 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA) and dopamine (DA) in hippocampus. Western blotting assay was used to detect the expression levels of DJ-1, PI3K, AKT, phosphorylated PI3K (p-PI3K), phosphorylated AKT ( p-AKT), Bcl-2 and Bcl-2 associated X protein ( Bax) in the hippocampus ofrats. Results Overexpression of DJ-1 significantly reduced the cell apoptosis rate in hippocampusand the levels of TNF-α and IL-6 in serum and the expression level of Bax in hippocampus, and upregulated the levels of 5-HT, 5-HIAA and DA in hippocampus and the expression levels of p-PI3K, p-AKT and Bcl-2 in hippocampus. However, the PI3K inhibitor LY294002 could partially reversethe protective effect of DJ-1 overexpression on neurons. Conclusion Overexpression of DJ-1 couldsignificantly inhibit inflammatory stress in the hippocampus of depression rats, reduce the apoptosis rate of neurons in the hippocampus, upregulate the levels of 5-HT, 5-HIAA and DA in the hippocampus, the mechanism may be related to the activation of PI3K / AKT signaling pathway. Related Articles | Metrics Select MYH11 Activates the ERK / MAPK Signaling Pathway and Induces Growth and Metastasis of Laryngeal Squamous Cell Carcinoma Cells #br# ZHONG Huacai, ZHENG Yuebin, YANG Yirong, YAN Bincheng, YI Wang, WANG Qian, WU Jun Journal of Medical Molecular Biology    2025, 22 (1): 62-67.   DOI: 10.3870/j.issn.1672-8009.2025.01.010 Abstract （112）      PDF （3440KB）（217）       Knowledge map    Save Objective To investigate the effect and mechanism of myosin heavy chain 11( MYH11 ) on the malignant biological behaviors of laryngeal squamous cell carcinomacells. Methods qRT-PCR was used to detect the expression level of MYH11 mRNA in laryngealsquamous cell carcinoma tissues and cells. Laryngeal squamous cell carcinoma cells TU686 were divided into 2 groups: si-MYH11 group and si-NC group. FD-LSC-1 cells were divided into 2 groups: MYH11 group and Vector group. CCK8, flow cytometry, wound-healing assay and Transwell assay were used to determine the cell proliferation, apoptosis, migration, and invasion abilities, respectively. Western blotting was used to detect the phosphorylation level of ERK1 / 2 and the expressionlevel of MAPK in each group of cells. Results MYH11 was highly expressed in laryngeal squamouscell carcinoma tissues and cells. The proliferation, migration, and invasion ability of TU686 cells inthe si-MYH11 group were significantly lower than those in the si-NC group ( P < 0. 05), and cell apoptosis was significantly higher than that in the si-NC group (P < 0. 01), the ERK1 / 2 phosphorylation level and MAPK expression level were significantly lower than those in the si-NC group (P< 0. 01). The proliferation, migration, and invasion ability of TU686 cells in the MYH11 groupwere significantly higher than those in the Vector group (P < 0. 05), and cell apoptosis was significantly lower than that in the Vector group ( P < 0. 01), the phosphorylation level of ERK1 / 2 and MAPK expression level were significantly higher than those in the Vector group (P < 0. 01). Conclusion MYH11 activates the ERK/ MAPK signaling pathway and promotes the proliferation, migration, and invasion of laryngeal squamous cell carcinoma cells. Related Articles | Metrics Select Causal Relationship Between Gut Microbiota and Vitamin D Deficiency: A Two-sample Mendelian Randomization Study #br# GUO Jing, LUO Jiamei , ZHU Junyong Journal of Medical Molecular Biology    2025, 22 (1): 68-75.   DOI: 10.3870/j.issn.1672-8009.2025.01.011 Abstract （151）      PDF （5302KB）（152）       Knowledge map    Save Objective To investigate the association between gut microbiota and vitamin D deficiency, and to identify specific gut microbial taxa related to the risk of vitamin D deficiency. Methods Data from genome-wide association studies (GWAS) on gut microbiota and vitaminD deficiency were summarized and analyzed. Inverse variance weighted (IVW) method was used for Mendelian randomization analysis to assess the causal relationship between gut microbiota taxa and vitamin D deficiency. Sensitivity analyses were conducted to evaluate heterogeneity, pleiotropy, androbustness of the results. Results In the absence of heterogeneity and horizontal pleiotropy, the IVW analysis method that showed Holdemania ( OR = 1. 524, 95 % CI = 1. 001-2. 231, P = 0. 049), Allisonella (OR = 1. 597, 95 % CI = 1. 095-2. 329, P = 0. 015), Escherichia-Shigella (OR = 2. 000, 95 % CI = 1. 156-3. 463, P = 0. 013), and Lachnospiraceae NC2004 group (OR = 2. 106, 95 % CI = 1. 178-3. 766, P = 0. 012) were positively associated with the risk of vitamin D deficiency. While the Lachnospira (OR = 0. 324, 95 % CI = 0. 124-0. 844, P = 0. 021) and Tyzzerella3 (OR = 0. 591, 95 % CI = 0. 406-0. 861, P = 0. 006) were negatively associated with the risk of vitamin D deficiency. Conclusion This study found significant correlations between the abundance of certain specific strains in the gut microbiota and the risk of vitamin D deficiency. This discovery may provide new potential targets for the prevention and treatment of vitamin D deficiency. Related Articles | Metrics Select Identification of Differentially Expressed Glycolysis-related Genes and Establishment of Prognostic Model for Gastric Cancer by Bioinformatics #br# XU Juan, HU Wanqi Journal of Medical Molecular Biology    2025, 22 (1): 76-83.   DOI: 10.3870/j.issn.1672-8009.2025.01.012 Abstract （184）      PDF （5658KB）（366）       Knowledge map    Save Objective To explore the expression of glycolysis-related genes ( GRGs) in gastric cancer by bioinformatics, and the relationship between the established risk scoring model andprognosis of gastric cancer. Methods The genes expression profiles and clinical feature data of gastric cancer samples were downloaded from the Cancer Genome Atlas (TCGA) database. The GRGs set was obtained from the GSEA database. We used “ limma” packets to identify differentially expressed GRGs in gastric cancer tissues, and used univariate Cox regression analysis to screen for prognosis related GRGs. Then, LASSO regression analysis was used to construct a prognosis prediction model based on the GRGs. A nomogram was developed based on the independent prognostic risk factors determined by Cox regression analysis. Finally, the correlations between 22 types of infiltrating immune cells and the GRGs or risk scoring models were analyzed. Results Twenty-one differentially expressed GRGs were identified, which were mainly enriched in the alcohol metabolism andtyrosine metabolism pathways. Finally, 5 prognostic related glycolytic genes ( ADH1B, ADH4, CLDN9, VCAN, and LHX90) were selected by LASSO and Cox models and were used to constructa gene signature for gastric cancer prognosis prediction. The overall survival of gastric cancer patients with low-risk scores is significantly better than that of gastric cancer patients with high-risk scores. The ROC curve analysis showed that the values of area under the curve (AUC) of the abovemodel to predict the 1-year, 3-year, and 5-year survival for the gastric cancer patients were 0. 602,0. 680, and 0. 802, respectively. The effectiveness of this model to predict the survival of gastriccancer patients was better than that of using tumor staging and grading. Univariate and multivariate Coxanalysis showed that the prognostic model, age, gender, tumor stage and tumor grade were independent prognostic factors for gastric cancer. Based on these prognostic factors, a Nomogram was constructed to predict the survival of gastric cancer patients. Finally, we found that the proportion of CD8T cells and helper follicular T cells was significantly reduced in the high-risk group, while the proportion of M0 macrophages and M2 macrophages was significantly higher in the high-risk group than inthe low-risk group. The proportion of helper follicular T cells was negatively correlated with the expression levels of ADH1B and VCAN and the risk scores. The proportion of M2 macrophages was positivelycorrelated with the expression level of VCAN and the risk scores. Conclusion The 5 GRGs screenedout in this study are related to the prognosis of gastric cancer, which can be used for the prognosis ofgastric cancer patients and may be used as potential therapeutic targets for gastric cancer. Related Articles | Metrics Select Research Progress on Application of Helminth Proteomics #br# YI Ling, PENG Peiying, HE Ping, Journal of Medical Molecular Biology    2025, 22 (1): 84-90.   DOI: 10.3870/j.issn.1672-8009.2025.01.013 Abstract （133）      PDF （723KB）（313）       Knowledge map    Save Proteomics studies the composition, structure, function, and interactions of allproteins in living organisms. Helminth infections have a serious impact on the health of hundreds of millions of people worldwide and result in significant economic losses for the livestock industry. With the continuous development and in-depth study of proteomics technologies, remarkable progress has been made in the application researches of helminth proteomics. This review summarizes the representative researches on helminth proteomics, the progress of proteomics technology studies, and the application on diagnosis, prevention, and control of helminthiasis, to provide new ideas and methods for screening diagnostic markers and drug targets for helminthiasis. Related Articles | Metrics Select The Role of Astrocytes in Subarachnoid Hemorrhage #br# SUI Chen, SUN Xingang Journal of Medical Molecular Biology    2025, 22 (1): 91-96.   DOI: 10.3870/j.issn.1672-8009.2025.01.014 Abstract （874）      PDF （719KB）（202）       Knowledge map    Save Subarachnoid hemorrhage (SAH) is a cerebrovascular disease that is characterizedby a high rate of disability and mortality. Astrocytes play a crucial role in brain injury and recovery following SAH. This paper summarizes the activation and polarization of astrocytes after SAH, their participation and mediation in early brain injury and delayed cerebral ischemia after SAH, and the extensive crosstalk between astrocytes and other brain cells, such as neurons, microglia, and vascular endothelial cells after SAH. In addition, the relevant targets and therapeutic methods for regulating astrocyte function after SAH are also listed here, offering some novel strategies for future translational therapies to alleviate the severe consequences of SAH. Related Articles | Metrics Select Research Progress on Azole Resistance in Aspergillus fumigatus Efflux Pumps #br# WANG Juan, MA Yan Journal of Medical Molecular Biology    2025, 22 (1): 97-100.   DOI: 10.3870/j.issn.1672-8009.2025.01.015 Abstract （250）      PDF （707KB）（114）       Knowledge map    Save Aspergillus fumigatus ( A. fumigatus) is an opportunistic pathogen widely found innature and can cause invasive aspergillosis (IA), with a high mortality rate in immunocompromisedpatients. Triazoles are the first-line therapy for IA, but in recent years, the number of azole-resistant Aspergillus fumigatus isolates is increasing worldwide, which greatly threatens the life and healthof patients. Efflux pumps are composed of transmembrane proteins that can expel unwanted substances out of cells, which is an important mechanism in protecting microorganisms. In addition, many studies suggest that efflux pumps can also mediate microbial drug resistance. This paper summarizes the recent progress on the function and regulation mechanism of the drug efflux pump ofA. fumigatus, which provides a theoretical basis for the deep understanding of the resistance mechanism in A. fumigatus and the screening of new targets of anti-infective drugs. Related Articles | Metrics Select In Vitro Study of miR-490-5p Regulating Inflammation and Angiogenesis in Hypoxy-induced Laryngeal Carcinoma FaDu Cells #br# TAN Yuanyuan, Aihemaitijiang Ailijiang, ZHOU Huiyin Journal of Medical Molecular Biology    2025, 22 (2): 101-107.   DOI: 10.3870/j.issn.1672-8009.2025.02.001 Abstract （156）      PDF （2251KB）（182）       Knowledge map    Save Objective To investigate the effect and molecular mechanism of microRNA-490-5p(miR-490-5p) on inflammatory response and angiogenesis in human laryngeal cancer cells inducedby hypoxia. Methods The human hypopharyngeal squamous cell carcinoma cell line FaDu was divided into 4 groups: control group (cultured in normoxic environment), hypoxic group (cultured in hypoxic environment), hypoxic + NC group (cultured in hypoxic environment and then transfected with mimics NC), and hypoxic + miR-490-5p group (cultured in hypoxic environment and then transfected with miR-490-5p mimics). The expression level of miR-490-5p in cells was detected by RT-qPCR, the cell proliferation activity was detected by CCK-8 method, the levels of tumor necrosis factor-α (TNF-α), interleukin (IL) -1β and IL-6 in the cell supernatant were determined by ELISA, the expression levels of proteins related to the nuclear factor κB (NF-κB) pathway in cellswas detected by Western blotting, the number of HUVEC tubes formed was detected by in vitro angiogenesis assay, the expression levels of vascular endothelial growth factor ( VEGF), epidermalgrowth factor ( EGF) and hypoxia-inducible factor-1α ( HIF-1α) in cells was detected by RTqPCR and Western blotting. Results Compared with those in the control group, the relative expression level of miR-490-5p in the hypoxia group was down-regulated (P < 0. 05), the proliferative activity was increased (P< 0. 05), the levels of TNF-α, IL-1β and IL-6 in supernatant were increased ( P < 0. 05 ), the relative expression levels of phosphorylated NF-κB P65 ( p-NF-κB P65) and phosphorylated IκB kinase α (p-IκBα) were up-regulated (P < 0. 05), and the number of HUVEC tubes was increased (P< 0. 05), the mRNA and protein relative expression levels of VEGF, EGF and HIF-1α were up-regulated (P< 0. 05). Compared with those in the hypoxia + NCgroup, the relative expression level of miR-490-5p in the hypoxia + miR-490-5p group was up-regulated (P< 0. 05), the proliferation activity was decreased (P < 0. 05), and the levels of TNF-α, IL-1β and IL-6 in supernatant were decreased (P< 0. 05), the relative expression levels of p-NF-κB P65 and p-IκBα were down-regulated, while the number of HUVEC tube formation was decreased (P< 0. 05 ), and the mRNA and protein expression levels of VEGF, EGF and HIF-1α were also down-regulated (P< 0. 05). Conclusion  Under hypoxic conditions, overexpression of miR-490-5p can inhibit the inflammatory response of laryngeal cancer cells and reduce the formation of tumor blood vessels. Related Articles | Metrics Select Bioinformatics Analysis of DHCR7 in Colon Cancer and Its Functional Validation #br# BAI Xiaogang, #, WANG Yanfeng, #, LIU Yongcheng, JI Haitao, Δ, ZHANG Jing Journal of Medical Molecular Biology    2025, 22 (2): 108-116.   DOI: 10.3870/j.issn.1672-8009.2025.02.002 Abstract （149）      PDF （8475KB）（59）       Knowledge map    Save Objective To explore the effects and regulatory mechanisms of dehydrocholesterolreductase 7 ( DHCR7) on the proliferation, apoptosis, migration, and invasion ability of coloncancer (CC) cells. Methods Using bioinformatics methods to analyze the relationship betweenDHCR7 expression and immune infiltration, prognosis, and sensitivity to anti-tumor drugs in colon cancer. qRT-PCR, Western blotting, and IHC were used to detect the mRNA and protein expression levels of DHCR7. Effect of DHCR7 knock-down on cell proliferation, cell cycle and apoptosis, cell migration and invasion was determined by MTT and colony formation assay, flow cytometry, wound-healing and Transwell assay, respectively. The key signaling pathways regulated by DHCR7were screened out through gene enrichment analysis and validated by Western blotting. Results  Bioinformatics analysis shows that the high expression of DHCR7 in colon cancer tissues was associated with the N-stage, specific survival, progression free survival, tumor immune infiltration level, and drug sensitivity of colon cancer. DHCR7 expression was upregulated in colon cancer tissues and cell lines. Knockdown of DHCR7 expression inhibited the proliferation, migration, and invasion of HCT166 cells. Wnt signaling pathway was one of the key signaling pathways regulated by DHCR7 inCC, and knockdown of DHCR7 inhibited Wnt signaling pathway. Conclusion DHCR7 regulatesthe Wnt signaling pathway to promote EMT in colon cancer cells, thereby promoting proliferation, migration, and invasion of HCT116 cells. Related Articles | Metrics Select Effect of LINC00365 on Proliferation, Apoptosis, Migration, and Invasion of Thyroid Cancer Cells by Targeting miR-519d #br# Wufuer Yimaer, WANG Huguo, Daerhan Sailikebieke, DENG Chao, MaYire Nuermaimaiti Journal of Medical Molecular Biology    2025, 22 (2): 117-123.   DOI: 10.3870/j.issn.1672-8009.2025.02.003 Abstract （190）      PDF （4029KB）（174）       Knowledge map    Save Objective To investigate the effects and mechanisms of LINC00365 on proliferation, apoptosis, migration and invasion of thyroid cancer cells. Methods qRT-PCR was used todetect the relative expression level of LINC00365 in thyroid cancer tissues and thyroid cancer celllines. Thyroid cancer cells BHP-10-3 were divided into 5 groups: siNC group, si-LINC00365 group, si-LINC00365 + NC inhibitor group, si-LINC00365 + miR-519d inhibitor group, and blank group. Dual luciferase reporter gene experiment was used to detect the targeting relationship between LINC00365 and miR-519d. Cell proliferation ability was detected by CCK8, cell migration abilitywas detected by wound healing assay, cell invasion ability was detected by transwell assay, apoptosis rate was detected by flow cytometry. Results The relative expression level of LINC00365 were significantly upregulated in thyroid cancer tissues and thyroid cancer cells. miR-519d is the target gene of LINC00365. the proliferation, migration, and invasion abilities of BHP-10-3 in the siLINC00365 group and the si-LINC00365 + NC inhibitor group were significantly reduced ( P <0. 05), and the cell apoptosis rate was significantly increased ( P < 0. 01) when compared withthose in the blank group. The proliferation, migration, and invasion abilities of BHP-10-3 in the siLINC00365 + miR-519d inhibitor group were significantly increased (P < 0. 05), and the cell apoptosis rate was significantly reduced (P < 0. 01) when compared with those in the si-LINC00365 group. Conclusion LINC00365 can target miR-519d to affect the proliferation, migration, invasion and apoptosis of thyroid cancer cells. Related Articles | Metrics Select Liensinine Induces Apoptosis in Glioma U251 Cells through ROS / JNK Pathway #br# LI Chengke, HE Qin, LUO Xiaoquan, FENG Hao, QIAO Fei Journal of Medical Molecular Biology    2025, 22 (2): 124-130.   DOI: 10.3870/j.issn.1672-8009.2025.02.004 Abstract （168）      PDF （5011KB）（412）       Knowledge map    Save Objective To investigate the effect of liensinine (LI) on apoptosis of U251 gliomacells and its mechanisms. Methods U251 and HEB cells were treated with different concentrationsof LI for 24 / 48 h, CCK8 assay and colony formation assay were performed to detect cell viability, flow cytometer was performed to detect apoptosis, and the expression levels of apoptotic proteins (Bax / Bcl-2, cleaved PARP) were detected by Western blotting. Cells were divided into 6 groups: control, LI, NAC, LI + NAC, SP600125, LI + SP600125. ROS was detected by DCFH-DA and p-JNK / cleaved PARP by Western blotting. U251 xenograft model was established to evaluate theeffect of LI on tumor volume / weight and tumor cell apoptosis. Results LI significantly inhibited theproliferation of U251 cells, decreased the colony formation of U251 cells, and promoted apoptosis. LI (80 μmol / L) induced ROS production and JNK phosphorylation, which were reversed byNAC and SP600125. In vivo experiments showed that LI inhibited tumor growth, reduced Ki67 positive cells, and promoted apoptosis. Conclusion LI selectively inhibits U251 via ROS / JNK-mediated apoptosis, demonstrating therapeutic potential for glioma. Related Articles | Metrics Select Multi-omics Analysis and Validation of a Mouse Model of Diabetes Mellitus with Behavioral Abnormalities Based on High-throughput Mass Spectrometry #br# YANG Shufang, ZHANG Haoqiang, CHEN Xi, FAN Lin, YU Yefan, WANG Shaohua Journal of Medical Molecular Biology    2025, 22 (2): 131-138.   DOI: 10.3870/j.issn.1672-8009.2025.02.005 Abstract （215）      PDF （4692KB）（109）       Knowledge map    Save Objective To screen and verify the differentially expressed protein and the metabolites in a mouse model of type 2 diabetes mellitus with cognitive behavior abnormalities by highthroughput mass spectrometry. Methods High-throughput mass spectrometry was used to detect thelevels of hippocampal tissue protein expression and serum metabolites in the DB group ( abnormal cognitive behavior group) and the M group (normal cognitive behavior group). Target proteins and metabolites were screened out by bioinformatics and were then verified through Western blotting andELISA. Results ① 45 proteins and 119 positive ion-and 110 negative ion-metabolites were found tobe significantly expressed, and KEGG analysis showed that the differentially expressed genes were enriched in multiple metabolic pathways. ② Correlation analysis showed that serotonin-containing synapses and purine metabolism pathways were pathways co-enriched by multi-omics analysis. ③ pyruvate kinase L / R ( PKLR )、 arachidonic acid ( AA ) and adenosine 5′-monophosphate, (AMP) were differentially expressed. Conclusion PKLR, AA and AMP may be used as potentialbiomarkers for the diagnosis of type 2 diabetes mellitus with cognitive dysfunction. Related Articles | Metrics Select miR-24 Acts as Spongy of S100A8 in Kidney Tubular Epithelium Exosomes to Enhance Mitochondrial Damage and Promote Kidney Stone Disease #br# Diyaer Dilimulati, BAI Junbo, LIU Kaifang, Nafeisa Tuerdi, LI Jia Journal of Medical Molecular Biology    2025, 22 (2): 139-145.   DOI: 10.3870/j.issn.1672-8009.2025.02.006 Abstract （153）      PDF （1403KB）（831）       Knowledge map    Save Objective To investigate theeffect of miR-24 and S100A8 in exosomes of an in vitro kidney stone cell model on kidney stone disease and the underlying mechanism. Methods Human proximal tubular epithelial HKC-8 cells were used to establish a kidney stone cell model in vitro. HKC-8 cells were divided into four groups: the control group, the model group, the miR-24mimic + model group (miR-24 mimic was transfected into the cells of the model group), and the mimic NC + model group (mimic NC was transfected into the cells of the model group). Bioinformatics analysis was performed to analyze the relationship of miR-24 and S100A8 3′-UTR by using TargetScan v7. 2. Dual luciferase reporter assay was used to verify the direct interactions between miR-24 and S100A8 3′-UTR. Exosomes were extracted. The levels of miR-24 in exosomes was determined by qPCR. Western blotting was used to determine the protein expression levels of CD9, CD63 and S100A8 in exosomes, and the protein expression levels of PINK1, Parkin and Cytochrome C (Cyt-C) in cells. The levels of inflammatory cytokines TNF-α, IL-1β and IL-6 in cell supernatants and malondialdehyde ( MDA) in cells were determined by ELISA. The levels of reactive oxygenspecies ( ROS) were determined by DCFH-DA fluorescent dye method. Results Dual luciferasereporter assays had proved a direct interactions between miR-24 and S100A8 3′-UTR. miR-24 wasdown-regulated and S100A8 was up-regulated in the exosomes of the Model group (P< 0. 05), the expression levels of mitophagy markers of PINK1, Parkin and Cytochrome C were up-regulated (P<0. 05), the intracellular ROS and MDA levels were up-regulated (P< 0. 05), TNF-α, IL-1β andIL-6 were up-regulated in cell supernatants in the Model group ( P < 0. 05) when compared withthose in the Control group. The above indexes were all partially reversed in the miR-24 mimic + Model group (P< 0. 05), while there had been no significant difference in the mimic NC + Model group(P > 0. 05) when compared with those in the Model group. Conclusion MiR-24 was down-regulated and as “spongy” of S100A8 in exosomes of kidney stone cell model to up-regulate S100A8 expression, enhance mitochondrial damage and promote kidney stone disease. Related Articles | Metrics Select Stromal Cells through Macrophage-Mediated Pathways in the Pathogenesis of Endometriosis #br# CAO Wenchao Journal of Medical Molecular Biology    2025, 22 (2): 146-152.   DOI: 10.3870/j.issn.1672-8009.2025.02.007 Abstract （130）      PDF （4210KB）（84）       Knowledge map    Save Objective To investigate the effect of halofuginone (HF) on proliferation and apoptosis of endometriotic stromal cells ( ESCs) in endometriosis ( EMs) by regulation of macrophage polarization through peroxisome proliferator-activated receptor gamma ( PPARG) -leukemiainhibitory factor ( LIF) axis. Methods Normal endometrial stromal cells ( NESCs) and ectopicendometrial stromal cells ( EESCs) were treated with different concentrations of HF. CCK8 assay was used to detect the cell proliferation activity, and TUNEL assay was used to detect the cell apoptosis. Bioinformatics analysis was performed to identify the intersection of targets of HF, EMs, and macrophage. A co-culture system of macrophages and EESCs was established, cells were then divided into 7 groups: M0 + EESCs group、 M2 + EESCs group、 M2 + EESCsHF group、 M0 + EESCs oe-PPARG group、 M0 + EESCssh-PPARG group、 M0 + EESCsoe-PPARG + oe-LIF group、 M0 + EESCsoe-PPARG + HF group. ELISA was used to detect the concentrations of M1 macrophage markers (iNOS, IL-6) and M2 macrophage markers (Arg-1, TGF-β) in the cell supernatant. CCK8 and TUNEL assay wereused to detect the proliferation and apoptosis of EESCs, respectively. Results HF had no significant effect on the proliferation activity of NESCs (F = 0. 195, P = 0. 959), but significantly inhibited the proliferation of EESCs and promoted cell apoptosis (P< 0. 05). The levels of iNOS and IL-6 in the M2 + EESCs group were decreased when compared with those in the M0 + EESCs group,while the levels of Arg-1 and TGF-β were increased. In addition, the proliferation activity of EESCswas increased and the apoptosis was decreased. HF intervention reversed the results above ( P <0. 05). PPARG was identified as a key target in this study through bioinformatics analysis and literature search. The levels of iNOS and IL-6 in the cell supernatant of the M0 + EESCsoe-PPARG group weredecreased, while the levels of Arg-1 and TGF-β were increased when compared with those in the M0 + EESCs group. The proliferation activity of EESCs were increased and apoptosis were decreased(P< 0. 05), while an opposite results were obtained in the M0 + EESCssh-PPARG group (P < 0. 05).Furthermore, upregulation of LIF expression or HF intervention in the M0 + EESCsoe-PPARG + oe-LIF andM0 + EESCsoe-PPARG + HF groups led to the increase of iNOS and IL-6 levels and proliferation activity ofEESCs, and the decrease of Arg-1 and TGF-β and apoptosis when compared with the M0 + EESCsoe-PPARGgroup (P < 0. 05). Conclusion HF inhibits M2 polarization of macrophages and inhibitsthe proliferation of EESCs while promoting cell apoptosis by regulating the PPARG-LIF signalingpathway. Related Articles | Metrics Select Effect of EPB41 Mediated Fatty Acid Oxidation on Esophageal Cancer Cell Proliferation and Migration #br# LIN Jinqiu, WANG Liang, LIU Shizhu Journal of Medical Molecular Biology    2025, 22 (2): 153-159.   DOI: 10.3870/j.issn.1672-8009.2025.02.008 Abstract （89）      PDF （4439KB）（66）       Knowledge map    Save Objective To investigate the effect of erythrocyte membrane protein band 4. 1(EPB41) on the malignant phenotype of esophageal cancer cells and explore the possible underlyingmechanisms based on fatty acid oxidation ( FAO) mediated by the Wnt / β-catenin signaling pathway. Methods KYSE30 cells and KYSE150 cells in logarithmic growth phase were divided into 5groups each. The mRNA and protein expression levels, cell proliferation and migration rate, ATPlevel, NADPH / NADP + ratio, reactive oxygen species ( ROS ) and GSH levels were detected. Results In KYSE30 cells, the number of cell clones, cell migration rate, ATP level, NADPH / NADP + ratio, ROS level, and protein expression levels of Wnt3a, β-catenin, and nuclear β- catenin in cells were significantly increased in the EPB41 siRNA group (P < 0. 05), and fatty acidoxidation inhibitor and Wnt pathway inhibitor could reverse the effect of EPB41. In KYSE150 cells, the number of clones, cell migration rate, ATP level, NADPH / NADP + ratio, ROS level, and the expression levels of Wnt3a, β-catenin, and nuclear β-catenin proteins were significantly reduced in the cells in the EPB41 overexpression group (P < 0. 05), and the effect of EPB41 could be reversed by the fatty acid oxidation inducer and the Wnt pathway activator. Conclusion EPB41 expression is down-regulated in esophageal cancer cells. EPB41 overexpression can inhibit the proliferation and migration of esophageal cancer cells by suppressing the FAO pathway, which may be achieved by modulating the Wnt / β-catenin signaling transduction. Related Articles | Metrics Select Protective Effect of Interfering with Rho-associated Coil Formation Protein Kinase 1 Expression on Mice with Acute Lung Injury #br# LI Yufang, YANG Nan, YU Xiaowei, WEI Zhiwei, ZUO Tianxin, ZOU Fang Journal of Medical Molecular Biology    2025, 22 (2): 160-165.   DOI: 10.3870/j.issn.1672-8009.2025.02.009 Abstract （97）      PDF （3239KB）（50）       Knowledge map    Save Objective To investigate the effect of interference with Rho-associated coil formingprotein kinase 1 on lung injury induced by lipopolysaccharide (LPS) in mice. Methods C57BL / 6mice were divided into 4 groups: healthy control group, model group, negative control group and ROCK1 interference group, 10 mice each group. Acute lung injury was induced with LPS (5 mg / kg, i. p. ). The expression level of ROCK1 was detected by RT-PCR and Western blotting. The pulmonary function detection system was used to detect the airway resistance, resting ventilation and lung volume in mice. HE staining was used to observe the pathological damage of lung tissues, and Masson staining was used to observe the pulmonary fibrosis. Western blotting was used to detect the protein expression levels of α-SMA, TGF-β1 and FN. TUNEL assay was used to detect the lung cellapoptosis. The levels of iNOS, IL-6 and TNF-α were detected by ELISA. Results ROCK1 washighly expressed in the model group and the lung injury was more serious when compared with thatin the healthy control group. ROCK1 interference group had lower expression level of ROCK1 (P <0. 05), and increased airway resistance, resting ventilation and lung volume when compared withthe model group (P < 0. 05). The pathological injury and degree of fibrosis in lung tissues were improved in the ROCK1 interference group, and the expression levels of α-SMA, TGF-β1 and FN proteins were significantly decreased (P< 0. 05). The number of apoptotic cells in lung tissues was significantly decreased (P< 0. 05), and the levels of iNOS, IL-6 and TNF-α in peripheral bloodwere significantly decreased in the ROCK1 interference group when compared with those in themodel group (P < 0. 05). Conclusion Interfering ROCK1 expression can improve lung function,pulmonary fibrosis, apoptosis and inflammation in LPS-induced acute lung injury mice. Related Articles | Metrics Select Knockdown of lncRNA LINC01296 Inhibited Proliferation and Stemcell Characteristics of Osteosarcoma Cells through Wnt / β-catenin Pathway #br# LIU Guangfei, GUO Zhiyuan, WANG Yanhua, LU Shouliang, GUO Lei, CHENG Cai Journal of Medical Molecular Biology    2025, 22 (2): 166-172.   DOI: 10.3870/j.issn.1672-8009.2025.02.010 Abstract （105）      PDF （2960KB）（69）       Knowledge map    Save Objective To investigate the effect of knocking down long non-coding RNA ( lncRNA) LINC01296 on the proliferation capacity and stem-cell characteristics of human osteosarcoma (OS) cells, and to explore the related mechanisms. Methods Human normal osteoblast cellline hFOB1. 19 and human OS cell lines MG63, U2OS and Saos2 were cultured, and the expression level of lncRNA LINC01296 was detected by qRT-PCR. MG63 cells were divided into 4 groups: control group, siRNA negative control group ( negative control siRNA was transfected into cells), LINC01296 siRNA interference group (LINC01296 siRNA was transfected into cells), LINC01296 siRNA + LiCl group ( LINC01296 siRNA was transfected into cells and cultured with 10 mmol / L Wnt / β-catenin pathway activator LiCl for 24 h). The expression level of lncRNA LINC01296 in each group was detected, the survival rate of cells in each group was detected by CCK-8 method, the proliferation of cells was observed by EdU staining, and the spheroid number in each group was detected by tumor cell spheroid formation assay, the expression levels of stem-cell related proteins (Nanog, OCT-4, SOX2) and Wnt / β-catenin pathway-related proteins (β-catenin, c-Myc, Cyclin D1) in cells of each group were detected by Western blotting. Results The relative expressionlevel of lncRNA LINC01296 in the human OS cell lines MG63, U2OS and Saos2 was significantlyhigher than that in the hFOB1. 19 cells (P< 0. 05). The survival rate, the proportion of EdU positive cells, and the number of tumor cell spheres of MG63 cells in the LINC01296 siRNA group wassignificantly decreased when compared with those in the control group (all P< 0. 05), in addition,the relative expression levels of Nanog, OCT-4, SOX2, β-catenin, c-Myc and Cyclin D1 in theLINC01296 siRNA group were significantly down-regulated (P< 0. 05). The survival rate, the proportion of EdU positive cells, and the number of tumor cell spheres of MG63 cells in theLINC01296 siRNA + LiCl group was significantly increased when compared with those in theLINC01296 siRNA group ( all P < 0. 05 ), at the same time, the relative expression levels ofNanog, OCT-4, SOX2, β-catenin, c-Myc and Cyclin D1 in the cells were significantly up-regulated (P< 0. 05). Conclusion Targeted knockout of lncRNA LINC01296 in OS cells can inhibit cellproliferation and reduce osteosarcoma cell stemness, which may be related to inhibiting the activation of Wnt / β-catenin pathway. Related Articles | Metrics Select Diagnostic Value of miR-425-5p in Endometrial Cancer and Effect of Inhibiting miR-425-5p on Proliferation, Migration and Apoptosis in Endometrial Cancer Cells #br# BAI Mihong, ZHANG Jie, KOU Li, WANG Jinbo Journal of Medical Molecular Biology    2025, 22 (2): 173-179.   DOI: 10.3870/j.issn.1672-8009.2025.02.011 Abstract （108）      PDF （2963KB）（73）       Knowledge map    Save Objective To analyze the diagnostic value of miR-425-5p in endometrial cancer(EC) and the effect of inhibiting miR-425-5p on the proliferation, migration, and apoptosis of ECcells. Methods The expression level of miR-425-5p in serum and tissues of patients with EC andbenign uterine lesions was detected by RT-qPCR, and was compared among patients with differentpathological characteristics of EC. The relationship between miR-425-5p expression in the tissues andserum and the pathological characteristics was analyzed, as well as its diagnostic value for EC. Theexpression level of miR-425-5p in normal endometrial epithelial hEEC cells, endometrial carcinomaIshikawa, HEC-1A, HEC-1B cells was detected by RT-qPCR. Ishikawa cells were divided into 3groups: Con group ( no treatment control), anti-miR-NC group ( transfected with anti-miR-425-5p) and anti-miR-425-5p group (transfected with anti-miR-425-5p). RT-qPCR was used to detect the miR-425-5p expression level. MTT and flow cytometry were used to detect cell proliferation, cell cycle and apoptosis. cell migration was detected by Transwell. The expression levels of CyclinD1,PCNA, Bax, Bcl-2 and MMP9 were detected by Western blotting. Results The expression level ofmiR-425-5p in serum and tissues of the endometrial carcinoma group was higher than that of the benign lesion group (P< 0. 05). There were statistically significant differences when comparing the expression level of miR-425-5p in patients with different lymph node metastasis statuses, FIGO stagesand degrees of differentiation (P< 0. 05). The expression of miR-425-5p in tissues and serum was positively correlated with FIGO stage, lymph node metastasis, and degree of differentiation ( r =0. 793, 0. 689, 0. 665, 0. 694, 0. 652, 0. 672, P < 0. 05). The AUC of miR-425-5p in tissuesand serum for the diagnosis of EC were 0. 782 and 0. 762, respectively. The sensitivities were74. 36 % , 71. 79 % , specificity, and the specificities were 71. 79 % , 70. 51 % , respectively. The expression level of miR-425-5p in endometrial carcinoma Ishikawa, HEC-1A, HEC-1Bcells was increased when compared with that in hEEC cells ( P < 0. 05). The expression level ofmiR-425-5p, cell activity, the proportion of cells in the S phase, the number of migrated cells,and the expression levels of Bcl-2, MMP9, CyclinD1 and PCNA proteins in the anti-miR-425-5pgroup were significantly decreased when compared with those in the anti-miR-NC group or the Congroup, while the proportion of cells in the G0 / G1 phase, the apoptosis rate and the protein expression of Bax were significantly increased (P < 0. 05). Conclusion miR-425-5p is highly expressedin EC tissues and serum, its expression level in EC tissues and serum is related to the patients’FIGO stage, lymph node metastasis and degree of differentiation. It has certain values in the diagnosisof EC. Moreover, inhibition of miR-425-5p can significantly inhibit the proliferation and migration ofEC cells, and induce cell apoptosis. Related Articles | Metrics Select Oridonin Improves Myocardial Ischemia-reperfusion Injury by Attenuating Endoplasmic Reticulum Stress-induced Apoptosis #br# YUAN Fang, SONG Haiping, WANG Congcong, HOU Binbin, HOU Aijun, ZHAO Weijin Journal of Medical Molecular Biology    2025, 22 (2): 180-186.   DOI: 10.3870/j.issn.1672-8009.2025.02.012 Abstract （118）      PDF （4184KB）（67）       Knowledge map    Save Objective To explore the effect of oridonin on myocardial ischemia-reperfusion injury. Methods A total of 108 rats were randomly divided into 6 groups: sham operation group, I /R group, low-dose, middle-dose and high-dose oridonin treatment groups (2. 5, 5 and 10 mg / kg, continuous intervention for 7 days before surgery) and positive control group (intravenous injection of alprostadil after modeling), with 18 rats in each group. The hemodynamic indicators, myocardial pathological injury, serum oxidative stress indicators, endoplasmic reticulum stress and apoptosisrelated mRNA and protein expression levels and the apoptosis of myocardial cells were detected. Results The oxidative stress indicator and hemodynamics were significantly improved in thehigh-dose oridonin treatment group and positive control group when compared with those in the I / Rgroup, and the myocardial infarction range and myocardial cell apoptosis rate were decreased (P <0. 05). The mRNA expression levels of endoplasmic reticulum stress-related genes were down-regulated (P < 0. 05), and the expression levels of apoptosis-related proteins were declined (P < 0. 05). Conclusion Oridonin can alleviate the myocardial injury in I / R rats, which may be related to alleviating oxidative stress injury and attenuating endoplasmic reticulum stress-induced apoptosis. Related Articles | Metrics Select Effect of Sodium Aescinate on Atherosclerosis and Antioxidant Activity in Hyperlipidemia Model Rats #br# WANG Xuezhi, HAO Yafeng, YUAN Tao, XU Zhenkun, GAO Shuxian Journal of Medical Molecular Biology    2025, 22 (2): 187-193.   DOI: 10.3870/j.issn.1672-8009.2025.02.013 Abstract （182）      PDF （2015KB）（30）       Knowledge map    Save Objective To investigate the effect of sodium aescinate on atherosclerosis and antioxidant activity in hyperlipidemia model rats and its mechanism. Methods Seventy-two SD ratswere randomly divided into 6 groups: control group, model group, sodium aescinate 0. 5 mg / kg group、 1 mg / kg、 2 mg / kg groups and atorvastatin calcium 10 mg / kg group. Except for the control group, hyperlipidemia rat model was established in the other five groups. After the corresponding drug treatments were administered to each group, the rats were sacrificed, and myocardial tissue sections were prepared for HE staining. The blood lipids, whole blood viscosity indicators, and oxidative stress indicators were detected by automatic biochemical analyzer, and the atherosclerosis index (AI) and index of HDL-C / TC were calculated. The expression of Keap1-Nrf2 / ARE signalingpathway related proteins in rats were detected by using Western blotting. Results The myocardialfiber arrangement in the sodium aescinate 1 mg / kg and 2 mg / kg groups and the atorvastatin calcium10 mg / kg group were more dispersed than that in the model group, the degree of nuclear lysis anddamage were improved, the levels of TC, TG and LDL-C were decreased, the level of HDL-C wasincreased, the final body weight and AI were decreased, and the value of HDL-C / TC was increased when compared with those in the model group. The whole blood viscosity and the plasma viscosity were decreased, the level of ApoA-I and SOD and GSH-Px were increased, the level ofApoB100 and MDA was decreased, and the protein expression levels of Keap1, NQO1, ARE andp-Nrf-2 / Nrf-2 were significantly increased (P < 0. 05). Conclusion Sodium aescinate can improvemyocardial histopathological injury, regulate dyslipidemia, resist atherosclerosis and inhibit oxidative stress in hyperlipidemia model rats, and its mechanism may be related to the activation of Keap1-Nrf2 / ARE signaling pathway. Related Articles | Metrics Select Application of miR-495-3p and Mn-SOD Gene Detection in Disease Evaluation of Diabetes Nephropathy Patients #br# ZHU Shuang, HU Xiao Journal of Medical Molecular Biology    2025, 22 (2): 194-199.   DOI: 10.3870/j.issn.1672-8009.2025.02.014 Abstract （119）      PDF （863KB）（24）       Knowledge map    Save Objective To explore the application value of gene detection of miR-495-3p andmanganese superoxide dismutase (Mn-SOD) in the disease evaluation of diabetes nephropathy patients. Methods A total of 150 patients with diabetes nephropathy who were treated in HuangshiCentral Hospital from January 2022 to December 2023 were selected, and another 150 patients with diabetes and 150 healthy people were included in this study as controls. the differences of miR-495-3p expression and Mn-SOD genotypes in each group were compared, and the value of miR-495-3p expression and Mn-SOD genotypes in predicting poor prognosis of diabetes nephropathy were analyzed. Results The expression level of miR-495-3p in the group of diabetes nephropathy patients was (0. 56 ± 0. 14), which was significantly lower than that of diabetes and healthy people (P<0. 05). There was a statistically significant difference in the distribution of genotypes at the 9 and5 777 loci of Mn-SOD gene in diabetes nephropathy, diabetes and healthy people (P< 0. 05). Theproportion of CT + CC genotype at the 9 loci of Mn-SOD gene in diabetes nephropathy was 40. 00 % ,the proportion of CT + CC genotype at position 5 777 of the Mn-SOD gene was 98. 00 % . The expression level of miR-495-3p in diabetes nephropathy patients with T2DM duration ≥ 10 years was(0. 46 ± 0. 14), which was significantly lower than that in patients with T2DM duration < 10 years(P< 0. 05). The expression level of miR-495-3p in patients with poor prognosis of diabetes nephropathy was (0. 47 ± 0. 14), which was significantly lower than that in patients with good prognosis(P< 0. 05). The proportion of CT + CC at Mn-SOD gene locus 9 genotype in patients with poor prognosis was 73. 33 % , which was significantly higher than that in patients with good prognosis (P <0. 05). There was no significant difference in CT + CC ratio of Mn-SOD gene 5 777 genotype betweenpatients with poor prognosis and those with good prognosis ( P > 0. 05). The area under the ROCcurve for predicting poor prognosis of miR-495-3p and Mn-SOD gene 9 locus genotypes was 0. 784(95 % CI: 0. 705 - 0. 863) and 0. 786 (95 % CI: 0. 700 - 0. 872), respectively ( P < 0. 05).Conclusion The level of miR-495-3p in patients with diabetes nephropathy is reduced, miR-495-3p expression and Mn-SOD genetypes have certain application values in predicting the prognosis ofdiabetes nephropathy. Related Articles | Metrics Select Signal Pathways Related to the Virulence of Aspergillus fumigatus under Stress Conditions #br# GAO Liang, MA Yan Journal of Medical Molecular Biology    2025, 22 (2): 200-204.   DOI: 10.3870/j.issn.1672-8009.2025.02.015 Abstract （126）      PDF （722KB）（152）       Knowledge map    Save Aspergillus fumigatus (A. fumigatus) is a common opportunistic pathogen. Its sporesare abundant in the human environment and are the main cause of invasive aspergillosis, with highinfection rate and mortality rate. The ability of A. fumigatus to resist and adapt to adverse environments is closely related to their virulence and is the key to the treatment of A. fumigatus infection. This review introduces the signal transduction pathways, including the unfolded protein response pathway, high osmolarity glycerolpathway, cell wall integrity pathway and calcium-calcineurin pathway, in A. fumigatus under different stress conditions and their effects on the growth,virulence and resistance to antifungal drugs. It provides new ideas for the development of innovative drugs for the treatment of invasive aspergillosis. Related Articles | Metrics Select Research Progress of Intestinal Macrophages in Pathogenesis of Inflammatory Bowel Disease #br# BO Jiajia, GUO Tingting, SHEN Huiqin Journal of Medical Molecular Biology    2025, 22 (2): 205-210.   DOI: 10.3870/j.issn.1672-8009.2025.02.016 Abstract （173）      PDF （708KB）（144）       Knowledge map    Save Inflammatory bowel disease ( IBD) is a class of chronic recurrent gastrointestinalinflammatory diseases caused by inflammation and immune system disorders. Its pathogenesis is complex, and the immune system attacks the lining of the intestine, causing chronic inflammation and tissue damage. As a typical inflammatory disease, multiple immune cell types are involved in the pathogenesis of IBD. Among them, macrophages are thought to play a pivotal role. Intestinal macrophages are an important part of maintaining intestinal immune homeostasis and inhibiting the inflammatory response, which is of great significance for the treatment of inflammatory bowel disease. Given that macrophages can coordinate inflammation resolution and tissue repair, they are currently considered an attractive target for developing new treatments for inflammatory bowel disease. This review summarizes the research progress of immunomodulatory role of intestinal macrophages in IBD, so as to provide reference for the research of pathogenesis and the clinical treatment of IBD. Related Articles | Metrics Select Protective Effect of Dihydrolycorine on Rats with CVB3-induced Viral Myocarditis #br# BAI Hongmin, YANG Yongzhong, CHEN Shujie, YANG Chao, LIU Wei Journal of Medical Molecular Biology    2025, 22 (3): 211-216.   DOI: 10.3870/j.issn.1672-8009.2025.03.001 Abstract （133）      PDF （7677KB）（131）       Knowledge map    Save Objective To explore the influence and mechanism of dihydrolycorine ( DL) onrats with viral myocarditis (VMC) induced by Coxsackie B3 virus (CVB3). Methods A total of72 SD rats were randomized into 6 groups: blank control group, model group, 10 mg / kg DLgroup, 20 mg / kg DL group, 40 mg / kg DL group, and Shenmai injection group (200 mg / kg),with 12 rats in each group. The CVB3-induced VMC model was established and intervened for 7days. The levels of serum myocardial enzymes and the hemodynamic indexes were detected. HE staining was used to detect the myocardial tissue pathological damage. TUNEL was used to detect myocardial cell apoptosis. Western blotting was applied to detect the expression levels of apoptosis andendoplasmic reticulum stress-related proteins. Results Compared with those in the model group,the pathological damage of myocardial tissue was alleviated, and the levels of serum myoglobin(Mb), creatine kinase isoenzyme MB (CK-MB) and cardiac troponin I (cTnI), the myocardialapoptosis rate and the protein expression levels of BCL2-associated X protein (Bax), C / EBP homologous protein (CHOP), glucose-regulated protein 78 ( GRP78) and GRP94 were reduced inthe 20 and 40 mg / kg DL groups and the Shenmai injection group ( P < 0. 05). Moreover, the leftventricular pressure (LVP), the maximum change rate of left ventricular pressure rise and fall ( ±dp / dtmax), and the protein expression levels of B-cell lymphoma-2 ( Bcl-2) and the cleaved /caspase-3 ratio rose in the 20 and 40 mg / kg DL groups and the Shenmai injection group ( P <0. 05). Conclusion DL can relieve the VMC myocardial injury and improve the cardiac dysfunction, which may be related to the inhibition of endoplasmic reticulum stress-mediated apoptosis. Related Articles | Metrics Select Effect of Olaparib on Survival, Epithelial-mesenchymal Transition, and Tumor Stem Cell-like Characteristics in Ovarian Cancer ES2 Cells #br# YE Jing, ZHAO Jinrong , LI Ping, HAN Ci, ZHANG Xin, CHENG Wei, TIAN Xiaoru Journal of Medical Molecular Biology    2025, 22 (3): 217-222.   DOI: 10.3870/j.issn.1672-8009.2025.03.002 Abstract （147）      PDF （4428KB）（109）       Knowledge map    Save Objective To explore the effect of olaparib on the survival, epithelial-mesenchymal transition ( EMT ) and tumor stem cell-like characteristics of ovarian cancer ES2cells. Methods Ovarian cancer ES2 cells were culturedin vitro, and they were divided into 5groups: control group, low-dose olaparib group, middle-dose olaparib group, high-dose olaparib group and doxorubicin 0. 5 μmol / L group. Cells proliferation, apoptosis, invasion and migration were detected by 5-ethynyl-2′-deoxyuridine ( EDU) staining, flow cytometry, Transwell assay, and wound healing assay, respectively. The epithelial-mesenchymal transition ( EMT) of cells was observed under light microscope, tumor stem cell-like characteristics were observed by tumor spheroid formation assay, and protein expression level was detected by Western blotting. Results Compared with those in the control group, the apoptosis rate of ES2 cells and the expression level of Ecadherin were significantly increased in the low-, middle-, high-dose olaparib group and doxorubicin 0. 5 μmol / L group ( P < 0. 05), the ratio of EDU staining positive cells, number of invasioncells per unit area, cell wound-healing rate, number of tumor spheroid, spheroid diameter, and the expression levels of nuclear antigen Ki67, Survivin, vascular endothelial growth factor(VEGF), N-cadherin, cluster of differentiation 44 (CD44) and aldehyde dehydrogenase 1 (ALDH1) were significantly decreased in the middle-and high-dose olaparib group and doxorubicin 0. 5μmol / L group (P< 0. 05). Conclusion Olaparib of over 30 mg / L can significantly inhibit proliferation, invasion, and migration of ovarian cancer ES2 cells, and promote their apoptosis, which may be through inhibition of Ki67 and regulation of EMT. Related Articles | Metrics Select CircITCH Regulates Proliferation and Invasion of Colorectal Cancer Cells via Targeting miR-106b #br# JIANG Linyan, SHEN Xiaowen, XU Meirong Journal of Medical Molecular Biology    2025, 22 (3): 223-228.   DOI: 10.3870/j.issn.1672-8009.2025.03.003 Abstract （161）      PDF （2758KB）（301）       Knowledge map    Save Objective To study the effect of circITCH on the proliferation, invasion of colorectal cancer cells via targeting miR-106b. Methods Colorectal cancer cell lines SW620, HT-29,HCT116, Caco-2, SW480, and normal colon epithelial cell line NCM460 were cultured. The expression levels of circITCH and miR-106b were detected, and HT-29 cells were selected for further experiments and were divided into 7 groups: Negative control ( NC) group, circITCH group, miR-NC group, miR-106b group, NC plasmid + miR-NC group, circITCH + miR-NC group, andcircITCH + miR-106b group. The A450 value, number of invasion cells and the expression levels of PTEN and B cell translocation gene 3 (BTG3) were detected. Results The expression level of circITCH in the SW620, HT-29, HCT116, Caco-2 and SW480 cells was lower than that in theNCM460 cell, while the expression level of miR-106b was higher in the NCM460 cell (P < 0. 05).Dual-luciferase reporter gene assay showed that miR-106b could bind with circITCH reporter gene). The expression levels of circITCH, PTEN, BTG3 in the circITCH group were higher than those inthe NC group, the expression level of miR-106b, A450 value, and the number of invasion cells were lower than those in the NC group (P < 0. 05). The expression level of miR-106b, A450 value, andthe number of invasion cells in the circITCH + miR-106b group were higher than those in the circITCH + miR-NC group, the expression levels of PTEN, BTG3 were lower than those in the circITCH + miR-NC group (P< 0. 05). Conclusion CircITCH can inhibit the proliferation and invasion of colorectal cancer cells via targeting miR-106b. Related Articles | Metrics Select Effect of Nrf2 on Brain Injury and Microglial Cell Polarization in Neonatal Hypoxic-ischemic Encephalopathy Rats #br# WU Zhishan, XIAO Pei, LI Yanliang, YU Zhanzhang Journal of Medical Molecular Biology    2025, 22 (3): 229-236.   DOI: 10.3870/j.issn.1672-8009.2025.03.004 Abstract （167）      PDF （8862KB）（51）       Knowledge map    Save Objective To investigate the effect of nuclear factor E2-associated factor 2 (Nrf2)on brain injury in neonatal hypoxic-ischemic encephalopathy ( HIE) rats. Methods The experiments were divided into 4 groupd: Sham group, HIE group, Sham + Nrf2 group, and HIE + Nrf2group, with 10 neonatal SD rats in each group. The HIE model was established, and unloaded adenovirus or adenovirus containing Nrf2 overexpression vector was transfused into the ventricle. After 14days, cerebral infarction was detected by 2, 3, 5 triphenyltetrazolium chloride ( TTC) staining, and brain histopathological changes were observed by Hematoxylin-eosin (HE) staining. The levels of tumor necrosis factor-α (TNF-α), interleukin-1β ( IL-1β), interleukin-6 (IL-6), and interleukin-10 ( IL-10 ) in brain tissues were determined by enzyme-linked immunosorbent assay (ELISA). The proportion of M1-type microglia labeled with ionized calcium binding adaptor molecule-1 (Iba-1) / inducible nitric oxide synthetase (iNOS) and the proportion of M2-type microglia labeled with Iba-1 / arginase 1 ( Arg-1) were detected by double-labeling immunofluorescence staining. The protein expression levels of iNOS, CD86, Arg-1, Macrophage mannose receptor(CD206), Nrf2, brain-derived neurotrophic factor (BDNF), and glia-derived neurotrophic factor(GDNF) were detected by Western blotting. Results Compared with those in the HIE group, thevolume of cerebral infarction in the HIE + Nrf2 group was significantly decreased, neuronal nucleus shrinkage was decreased, the levels of TNF-α, IL-1β and IL-6 in brain tissues were significantly decreased, and the levels of IL-10 were significantly increased, the proportion of Iba-1 + / iNOS + M1- type microglia was significantly decreased, and the proportion of Iba-1 + / Arg-1 + M2-type microglia was significantly increased, the expression levels of iNOS and CD86 protein in brain tissues were significantly down-regulated, the expression levels of Arg-1, CD206, Nrf2, BDNF and GDNF were significantly up-regulated (P < 0. 05). Conclusion Nrf2 can reduce neuroinflammation by promotingthe transformation of microglia from M1 type to M2 type to improve the brain injury of neonatal rats with HIE. Related Articles | Metrics Select Vitamin D3 Mediates TIPE2 in Regulation of Macrophage Function and Phenotype in Chronic Rhinosinusitis with Nasal Polyps #br# HUANG Xiaorong, TAN Hui, CHEN Juan, Kadiliya Mulati, ZHANG Jin, CHEN Lunjian Journal of Medical Molecular Biology    2025, 22 (3): 234-244.   DOI: 10.3870/j.issn.1672-8009.2025.03.005 Abstract （113）      PDF （1663KB）（93）       Knowledge map    Save Objective To investigate the regulatory role of vitamin D3 ( VD3 ) -mediatedtumor necrosis factor-alpha induced protein 8-like protein 2 ( TIPE2) on macrophage function andphenotype in chronic rhinosinusitis with nasal polyps (CRSwNP). Methods Peripheral blood samples were collected from patients with CRSwNP as the CRSwNP group, and from patients under went surgery for isolated nasal septal deviation as the Control group. RT-qPCR and Western blotting were used to detect the expression levels of TIPE2 and Arginase-1 ( Arg-1) in peripheral blood, andchemiluminescence was used to detect the changes in VD3 concentration in peripheralblood. J774A. 1 macrophages were cultured in vitro and divided into 5 groups: silenced TIPE2 (siTIPE2#2) group and its negative control ( si-NC) group, negative control for TIPE2 overexpression (oe-NC) group, oe-NC combined with VD3 treatment group ( oe-NC + VD3 group), and overexpressed TIPE2 recombinant vector ( oe-TIPE2 ) combined with VD3 treatment group ( oeTIPE2 + VD3 group). In addition, a mouse model of CRSwNP was established, with CRSwNP mice divided into 3 groups: empty vector treatment group (CRSwNP + empty vector group), CRSwNP + oeTIPE2 group, and CRSwNP + oe-TIPE2 + VD3 group. Peripheral blood and macrophages were collected fr om each group of mice. RT-qPCR and Western blotting were used to detect the expression levels of TIPE2 and Arg-1 in macrophages. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of interleukin ( IL ) -4 and IL-13 in cell culture supernatants and mouse sera in eachgroup. Results Compared to those in the control group, VD3 concentration was decreased in the CRSwNP group, while the expression levels of TIPE2 and Arg-1, as well as the serum concentrations of IL-4and IL-13, were upregulated (all P< 0. 05). There was a significant positive correlation between Arg-1 and TIPE2 levels (r =0. 994, P<0. 01), and both Arg-1 and TIPE2 levels were significantly negatively correlated with VD3 concentration (r = -0. 652, P<0. 01; r = -0. 745, P<0. 01). Compared to thosein the si-NC group, the expression levels of Arg-1 and IL-4 and IL-13 concentrations decreased in the siTIPE2#2 group (all P< 0. 05). Compared to those in the oe-NC group, the expression levels of TIPE2 and Arg-1, as well as IL-4 and IL-13 concentrations, decreased in the oe-NC + VD3 group (all P <0. 05). Moreover, compared to those in the oe-NC + VD3 group, the expression levels of TIPE2 and Arg-1, as well as IL-4 and IL-13 concentrations, increased in the oe-TIPE2 + VD3 group (all P < 0. 05).Compared to those in the CRSwNP + emptyvector group, the expression levels of TIPE2 and Arg-1 increased in the CRSwNP + oe-TIPE2 group, while VD3 concentration decreased and the serum concentrations of IL-4 and IL-13 increased (all P<0. 05). Compared to those in the CRSwNP + oe-TIPE2 group,the expression levels of TIPE2 and Arg-1 decreased in the CRSwNP + oe-TIPE2 + VD3 group, while theVD3 concentration increased and the serum concentrations of IL-4 and IL-13 decreased (all P<0. 05).Conclusion VD3 inhibits the expression of Arg-1, IL-4, and IL-13 in CRSwNP by downregulatingTIPE2 expression. Related Articles | Metrics Select Adipose Stem Cell-derived Exosomes Promote Osteogenic Differentiation of Periodontal Ligament Stem Cells through miR-654-3p #br# YANG Yimi, WANG Wei, CHEN Jiedian, AN Bingtao, WEN Ying Journal of Medical Molecular Biology    2025, 22 (3): 245-251.   DOI: 10.3870/j.issn.1672-8009.2025.03.006 Abstract （117）      PDF （5083KB）（53）       Knowledge map    Save Objective To investigate the effect of adipose stem cells-derived exosomes ( ADSCs-Exo) on osteogenic differentiation of periodontal ligament stem cells ( PDLSCs) through themiR-654-3p pathway. Methods Human ADSCs were isolated, identified, and cultured in vitro,and exosomes were isolated. Human PDLSCs were isolated in vitro, and the miR-654-3p inhibitor orits negative control (inhibitor NC) were transferred into cells, and cultured with or without a combined osteogenic induction solution. Cells were divided into 6 groups: Blank group, ADSCs-Exogroup, inhibitor NC group, inhibitor NC + ADSCs-Exo group, miR-654-3p inhibitor group, miR-654-3p inhibitor + ADSCs-Exo group. After 7 days of induction, the expression levels of miR-654-3p, osteocalcin ( OCN) and typeⅠ collagen ( COL1A1) mRNA in cells were detected by RTqPCR, and ALP activity was detected in cells by alkaline phosphatase (ALP) activity kit. After 21days of induction, the alizarin red staining method was used to detect the calcium nodules’ formation ability of cells, and the expression levels of OCN and COL1A1 protein were detected by West ern blotting. Results Compared with those in the Blank group or inhibitor NC group, the expression level of miR-654-3p, the activity of ALP, the expression levels of OCN and COL1A1 mRNAand protein in the ADSCs-Exo group were increased (P< 0. 05), and the formation ability of calcium nodules was enhanced (P < 0. 05), and the expression level of miR-654-3p was decreased inthe miR-654-3p inhibitor group. Compared with those in the inhibitor NC + ADSCs-Exo group, the ALP activity, the expression levels of OCN and COL1A1 mRNA and protein in the miR-654-3p inhibitor + ADSCs-Exo group were decreased (P < 0. 05), and the formation ability of calcium nodules was decreased ( P < 0. 05 ). Conclusion ADSCs-Exo promote osteogenic differentiation of PDLSCs by up-regulating the expression of miR-654-3p. Related Articles | Metrics Select Wutou Decoction Inhibits Inflammation and Oxidative Stress Induced Injury of Human Urogenic Stem Cells by Ahr/ LOC101928120 / SHC1 Signaling Pathway #br# WU Dan, TONG Liangming, LI Xi, ZHOU Ping, LI Jiefang Journal of Medical Molecular Biology    2025, 22 (3): 252-258.   DOI: 10.3870/j.issn.1672-8009.2025.03.007 Abstract （179）      PDF （2239KB）（69）       Knowledge map    Save Objective To investigate the mechanism by which Wutou decoction ( WTD) inhibits inflammatory and oxidative stress induced injury of human urogenic stem cells ( UdSC) bymodulating the aryl hydrocarbon receptor ( Ahr ) / long non-coding RNA ( LncRNA )LOC101928120 / SHC articulin 1 ( SHC1) signaling pathway. Methods UdSC cells were dividedinto 5 groups Control group, IL-1β group, IL-1β + WTD group, H2 O2 group, and H2 O2 + WTD group. CellTiterGlo assay and flow cytometry were applied to detect the proliferation and apoptosis in the cells of each group. qRT-PCR was applied to detect the expression levels of Ahr, LOC101928120, and SHC1 mRNA. Western blotting was applied to detect the expression levels of Ahr, HDAC1, SHC1, COL2, and SOX-9. ELISA was applied to detect the levels of IL-6, TNF-α, and MMP-13 in inflammation-induced UdSC cells. DCFH-DA fluorescent probe was applied todetect the ROS level in oxidative stress-induced UdSC cells. Results The A 560 nmvalue, the expression levels of Ahr mRNA and protein, LOC101928120, COL2, SOX-9 protein in the IL-1β group were lower than those in the Control group, and the values of above indexes in the IL-1β + WTDgroup were higher than those in the IL-1β group (P< 0. 05). The apoptosis rate, the levels of IL-6,TNF-α, MMP-13, and the expression levels of SHC1 mRNA and protein and HDAC1 protein in the IL-1β group were higher than those in the control group, and the values of above indexes in the IL-1β + WTD group were lower than those in the IL-1β group (P < 0. 05). TheA560 nm value, the expression levels of Ahr mRNA and protein, LOC101928120, COL2 and SOX-9 proteins in the H2O2 group were lower than those in the Control group, and the values of above indexes in the H2 O2 + WTD group were higher than those in the H2O2 group (P< 0. 05). The apoptosis rate, the proportion of ROS-positive cells, and the expression levels of SHC1 mRNA and protein and HDAC1 protein were higher than those in the Control group, and the above values in the H2 O2 + WTD groupwere lower than those in H 2O2 group (P< 0. 05). Conclusion WTD inhibits inflammatory and oxidative stress-induced injury in human UdSC, the mechanism may be achieved by modulating the Ahr / LOC101928120 / SHC1 signaling pathway. Related Articles | Metrics Select Immunomodulatory Effect of Tetramethylpyrazine on MCP-1 in Allergic Rhinitis Rats #br# CHENG Jie, WANG Wenguang Journal of Medical Molecular Biology    2025, 22 (3): 259-265.   DOI: 10.3870/j.issn.1672-8009.2025.03.008 Abstract （124）      PDF （5199KB）（146）       Knowledge map    Save Objective To investigate the immune regulatory effects of tetramethylpyrazine( TMP) on allergic rhinitis (AR) rats by regulating the MCP-1 / CCR2 signaling pathway. Methods Rats were randomly separated into 6 groups: Control group, Model group, TMP low-dose (TMP-L) group, TMP high-dose (TMP-H) group, TMP-H + rMCP-1 (recombinant MCP-1 protein) group, and loratadine group. AR rats were rated for their symptoms. The blood cell count method was applied to detect the number of various types of cells in the nasal lavage fluid of each group. Flow cytometry was applied to detect the levels of CD4 + , CD8 + , and CD4 + / CD8 + ratio in serum. ELISA was applied to detect serum levels of IL-10, IL-17, IL-6, interferon-γ ( IFN-γ), immunoglobulin (IgE), and allergenic mediator histamine (HIS). HE staining was applied to observe the pathological morphology of rat nasal mucosa. Western blotting was applied to detect the expression levels of aquaporins AQP1, AQP2, MCP-1, and CCR2 in nasal mucosa tissues. Results Compared with those in the Model group, the TMP-L, TMP-H and loratadine groups showed an obvious reduction in nasal mucosal tissue damage in rats, the symptom score of allergic rhinitis, numbers of eosinophils, neutrophils, lymphocytes, and macrophages in nasal lavage fluid, serum CD8 + level, IL-17, IL-6, IgE, HIS levels, and the expression levels of AQP1, AQP2, MCP-1, and CCR2 proteins in nasal mucosa tissues were decreased, and the serum CD4 + , CD4 + / CD8 + ratio, IL-10, and IFN-γ levels were increased (P< 0. 05). The values of above indexes in the TMPH and loratadine groups were at the same level (P > 0. 05). RMCP-1 could alleviate the improvement effect of TMP on AR rats (P < 0. 05). Conclusion TMP can reduce inflammation, alleviatenasal mucosal damage, and improve immune function in AR rats, which may be related to the inhibition of the MCP-1 / CCR2 signaling pathway. Related Articles | Metrics Select Expression and Clinical Prognostic Value of MCUR1 in Triple-negative Breast Cancer #br# FU Yuxing, PENG Qian, YANG Chaogang, Journal of Medical Molecular Biology    2025, 22 (3): 266-270.   DOI: 10.3870/j.issn.1672-8009.2025.03.009 Abstract （130）      PDF （1455KB）（94）       Knowledge map    Save Objective To analyze the expression of mitochondrial calcium uniporter regulator 1 (MCURl) in triple-negative breast cancer (TNBC) and its clinical significance. Methods  Immunohistochemistry was used to detect the expression of MCUR1 protein in TNBC tissues and corresponding adjacent tissues of 98 patients. The relationship between MCURl expression in tumor tissuesand patients’clinicopathological features and overall survival was further analyzed. Results  MCUR1was overexpressed in TNBC, and its expression level was significantly higher than that in the adjacent tissues (t = 34. 58, P < 0. 01). Clinicopathological analysis showed that high MCUR1 expression in TNBC was significantly correlated with tumor grade, T stage, and TNM stage ( P 0. 05,respectively). Further survival analysis showed that patients with high expression level of MCUR1had a lower overall survival rate than those with low expression level ( χ2 = 4. 591, P = 0. 032), which was an independent risk factor for poor prognosis of TNBC (HR = 2. 106, 95 % CI: 1. 013-5. 628, P = 0. 035). Conclusion  The expression of MCUR1 in TNBC tissues is up-regulated, andits high expression is associated with tumor progression and poor prognosis, which is a potential biomarker to evaluate the prognosis of TNBC patients. Related Articles | Metrics Select Role of SIRT3 in Children with Acute Myeloid Leukemia #br# REN Hua, HAO Qiang, GUO Li, ZHENG Suhua, WEI Lei Journal of Medical Molecular Biology    2025, 22 (3): 271-276.   DOI: 10.3870/j.issn.1672-8009.2025.03.010 Abstract （111）      PDF （1616KB）（127）       Knowledge map    Save Objective To explore the effect of silent information regulator 3 (SIRT3) in children with acute myeloid leukemia (AML). Methods The expression level of SIRT3 in bone marrow cells of AML children and peripheral blood leukocytes of healthy blood donor children was detected. SIRT3 expression was knocked down in AML cells. The cells’proliferation, apoptosis, oxidative stress indexes, and protein expression levels of the Wnt / β-catenin signaling pathway weredetected. Results Compared with those in the normal children group, the expression levels of SIRT3mRNA and protein were increased in the AML children group (P < 0. 05). After knocking down SIRT3expression in AML cells, the cells proliferation, the colony formation ability, the levels of glutathione (GSH) and superoxide dismutase (SOD), the total antioxidant capacity (T-AOC), the expression level of β-catenin, and the transcription activity of T cell factor / lymphocyte enhancer factor (TCF/ LEF) were decreased, while the apoptosis rate, the levels of reactive oxygen species (ROS), malondialdehyde (MDA) and phosphorylated glycogen synthase kinase 3β (p-GSK-3β) were increased (P<0. 05), the GSK-3β inhibitor TWS119 could partially reverse the above effects. Conclusion Knocking down SIRT3 can inhibit the growth of AML cells and increase oxidative stress level, which may berelated to the inhibition of Wnt / β-catenin signaling pathways. Related Articles | Metrics Select Predictive Value of a Nomogram Prediction Model Based on Aspartate Aminotransferase to Platelet Ratio for Short-term Prognosis of Cervical Cancer Patients After Surgery #br# CAI Qian, XIE Shuang, SONG Xiaoqing Journal of Medical Molecular Biology    2025, 22 (3): 277-282.   DOI: 10.3870/j.issn.1672-8009.2025.03.011 Abstract （123）      PDF （1450KB）（63）       Knowledge map    Save Objective To construct a predictive model for short-term postoperative prognosis ofcervical cancer patients based on the aspartate aminotransferase-to-platelet ratio index ( APRI).Methods A total of 112 patients diagnosed with cervical cancer and undergoing radical surgeryfrom January 2021 to August 2023 in Hubei Jianghan Oilfield General Hospital were included as the cervical cancer group, according to the inclusion and exclusion criteria. Additionally, 100 healthy women who underwent gynecological examinations during the same period were selected as the control group. During follow-up, cervical cancer patients were divided into a good prognosis group (81 cases) and a poor prognosis group (31 cases) based on their postoperative prognosis. General information was compared between the cervical cancer group and the control group, and clinical data from the cervical cancer group were collected to explore the risk factors affecting the short-term prognosis of cervical cancer patients after radical surgery. A nomogram model was constructed to predict the prognosis of cervical cancer patients after radical surgery. The ROC curve was used to analyze the predictivevalue of APRI for the short-term postoperative prognosis of cervical cancer patients. Results Compared with the control group, the cervical cancer group had higher APRI and high-risk HPV infection rates (P<0. 05). Significant differences were observed in tumor diameter, differentiation grade, FIGO stage, lymph node metastasis, AST, APRI, and HPV between the good prognosis group and thepoor prognosis group (all P<0. 05). Upon conducting Logistic regression analysis, it was determinedthat the following factors emerged as independent predictors of short-term unfavorable prognosis in cervical cancer patients following radical surgery: tumor diameter, degree of differentiation, FIGO stage, lymph node metastasis status, APRI values, and the presence of high-risk HPV infection (allP<0. 05). The calibration curve of the nomogram model indicated high applicability, with accurateand reliable predictions. The ROC curve results showed that APRI could serve as an effective diagnostic indicator for predicting short-term poor postoperative prognosis in cervical cancer patients (AUC =0. 743, P<0. 05). Conclusion APRI may have a reference value in predicting the short-term prognosis of cervical cancer patients undergoing radical surgery. Related Articles | Metrics Select Effect of ω-3 Polyunsaturated Fatty Acids on Wound Healingin Rats with Chronic Refractory Wounds #br# LI Xun, LI Desheng, CHEN Jie Journal of Medical Molecular Biology    2025, 22 (3): 283-289.   DOI: 10.3870/j.issn.1672-8009.2025.03.012 Abstract （127）      PDF （7866KB）（45）       Knowledge map    Save Objective To investigate the effect of ω-3 polyunsaturated fatty acids ( ω-3 PUFAs) on wound healing in rats with chronic refractory wounds. Methods SD rats were randomlyseparated into 6 groups: normal group, model group, ω-3 PUFAs low-, medium-, and high-dose groups, and Beifuxin group, with 10 rats in each group. Except for the normal group, the rats in the other groups were constructed with a chronic refractory wound model, and the wound healing ratio of the rats was measured after being treated with ω-3 PUFAs or Beifuxin. HE staining was used to determine the morphological structure of wound tissues. Immunohistochemical staining was used to detect the expression of Collagen Ⅱ and fibrin-binding protein (FN) and the expression of CD31 in the wound tissues to evaluate their microvascular density (MVD). ELISA detected the serum levels of pro-inflammatory factors TNF-α and IL-6. Western blotting was used to detect the expression levelsof pro-inflammatory factors and VEGF and TGF-β1 proteins in wound tissues. Results The levels ofTNF-α and IL-6, MVD, positive expressions of Collagen Ⅱ and FN, and the expression levels of TNF-α and IL-6, VEGF, TGF-β1 proteins in the model group were higher than those in the normalgroup (P < 0. 05). Compared with those in the model group, the levels of TNF-α and IL-6 and theprotein expression levels of TNF-α and IL-6 in the ω-3 PUFAs low-, medium-and high-dose groups and the Beifuxin group were decreased, the wound healing ratio, MVD, positive expressions ofCollagen Ⅱ and FN, the protein expression levels of VEGF and TGF-β1 were increased ( P < 0. 05). The changes in each index among ω-3 PUFAs groups were dose-dependent (P < 0. 05). No significant change was seen when compared those indexes between the Beifuxin group and the ω-3PUFAs high-dose group ( P > 0. 05). Conclusion  ω-3 PUFAs can inhibit wound inflammation,promote angiogenesis, and upregulate the expression of VEGF and TGF-β1, and promote the healing of chronic refractory wounds. Related Articles | Metrics Select Effect of Phillyrin on Streptozotocin-induced Diabetic Mice and Its Mechanism #br# MA Haiping, LI Hongling Journal of Medical Molecular Biology    2025, 22 (3): 290-294.   DOI: 10.3870/j.issn.1672-8009.2025.03.013 Abstract （189）      PDF （648KB）（114）       Knowledge map    Save Objective To explore the effect and mechanism of phillyrin on streptozotocin induced diabetic mouse model. Methods  A diabetic mouse Model was established and mice wererandomly divided into 6 groups: Control group, Model group, phillyrin low-dose group, phillyrin medium-dose group, phillyrin high-dose group, and metformin group. The blood glucose value was measured by a glucose meter. The glycosylated hemoglobin detector was used to detect glycosylated hemoglobin. The levels of serum urea nitrogen, creatinine, 24 h urine protein, and the levels of TC, TG, LDL-C, HDL-C, MDA, SOD and GSH-Px were detected by kits. The levels of TNF-α,IL-6, and IL-1β were detected by ELISA. Results Compared with those in the Control group, thelevels of serum urea nitrogen, creatinine and urine protein, the levels of TC, TG, LDL-C, thelevel of MDA content, and the levels of TNF-α, IL-6 and IL-1β were increased in the Modelgroup, while the level of HDL-C, and the levels of SOD and GSH-Px contents were decreased(P < 0. 05). Compared with those in the Model group, the levels of serum urea nitrogen, creatinineand urinary protein, the levels of TC, TG and LDL-C, the level of MDA content, and the levels of TNF-α, IL-6 and IL-1β were decreased in the phillyrin medium and high dose groups and metformin groups, while the level of HDL-C, and the levels of SOD and GSH-Px contents were increased.(P < 0. 05). Conclusion Phillyrin can protect streptozotocin-induced diabetic mice by regulation ofdyslipidemia, oxidative stress, and inflammation. Related Articles | Metrics Select Research Progress of Ferroptosis of Vascular Endothelial Cells in Atherosclerosis #br# ZHI Huimin, LI Yuanping, GAO Fen Journal of Medical Molecular Biology    2025, 22 (3): 295-299.   DOI: 10.3870/j.issn.1672-8009.2025.03.014 Abstract （220）      PDF （2761KB）（252）       Knowledge map    Save Atherosclerosis is the main pathological basis for cerebral infarction, coronary arteryatherosclerotic heart disease and other cardiovascular and cerebrovascular diseases. The abnormal death and functional disorder of vascular endothelial cells play an important role in it. Ferroptosis is a novel type of programmed cell death discovered in 2012, and there have been many studies showing that it plays an important role in the functional disorder and abnormal death of endothelial cells leading to AS. This review summarizes the mechanisms of ferroptosis and the possible mechanisms by which vascular endothelial cell ferroptosis leads to AS, and the drugs that may affect endothelial cell ferroptosis, providing a theoretical basis and research direction for the prevention and treatment of AS in clinical practice. Related Articles | Metrics Select Mechanism of Pimozide in Acute Myeloid Leukemia #br# #br# CHEN Chunxiao, LI Shuangyue, Journal of Medical Molecular Biology    2025, 22 (3): 300-304.   DOI: 10.3870/j.issn.1672-8009.2025.03.015 Abstract （117）      PDF （658KB）（277）       Knowledge map    Save Acute myeloid leukemia ( AML ) is a highly aggressive hematologicalmalignancy. Currently, chemotherapy and hematopoietic stem cell transplantation remain the primary treatment options for AML, yet approximately 30 % of patients experience relapse and have a poor prognosis. Pimozide, an antipsychotic drug, is primarily used in the treatment of schizophrenia, bipolar disorder, and other conditions. Several studies have now confirmed its antitumor effects. This article aims to review the mechanisms of pimozide in AML by literature analyzing, which provides insights into treatment strategies for AML. Related Articles | Metrics Select Pancreatic Ductal Infusion of gRNA Carried by Adeno-Associated Viruses for β-Cell Adra2a Gene Editing #br# #br# ZHANG Xin, WANG Xinxin, LYU Tingting, HAN Xiao, ZHU Yunxia Journal of Medical Molecular Biology    2025, 22 (4): 305-310.   DOI: 10.3870/j.issn.1672-8009.2025.04.001 Abstract （328）      PDF （6060KB）（116）       Knowledge map    Save Objective This study aims to utilize the CRISPR / Cas9 system to achieve β-cell specific gene knockout in the pancreas through adeno-associated virus ( AAV8 ) carrying guide RNA ( gRNA ) targeting the Adra2a gene. Methods  RIP2 ( rat insulin Ⅱ promoter ) -Cre; Cas9KI / + mice were used to achieve β-cell-specific gene editing. In this model, the RIP2 promoter drives Cre recombinase expression selectively in pancreatic β cells, resulting in targeted activation of Cas9 in these cells. To enable efficient editing of the Adra2a gene, adeno-associated virus serotype 8, a low-immunogenic vector, was used to deliver gene-specific guide RNAs. AAV8 particles carrying gRNAs targeting Adra2a were injected via the pancreatic duct, enabling precise geneknockout in β cells. Results   Successful β-cell-specific gene knockout was achieved in the pancreas, confirmed by tissue analysis, PCR, and protein expression analysis. GFP expression was observed in the pancreas, and the targeted gene was successfully disrupted in β cells. Conclusion  The use of AAV carrying gRNA in the RIP2-Cre; Cas9KI / + mouse model provides an effective method for β-cell-specific gene knockout, offering a valuable tool for future studies of islet gene function. Related Articles | Metrics Select Identification and Validation of Pathogenic Variants in FBN1 Gene for 7 Patients with Marfan Syndrome #br# #br# GUO Chen#, MAO Tiantian#, NA Heya, XU Hongen, TIAN Yongan, ZHOU Yuyang, CHANG Xin, LIU Danhua, GAO Chengshan Journal of Medical Molecular Biology    2025, 22 (4): 311-318.   DOI: 10.3870/j.issn.1672-8009.2025.04.002 Abstract （249）      PDF （4852KB）（114）       Knowledge map    Save Objective Seven patients with Marfan syndrome (MFS) were screened for pathogenic variants in the fibrinogen-1 (FBN1) gene to explore the relationship between MFS and FBN1 gene mutations. Methods Genomic DNA was extracted from the peripheral blood of 7 patients andthen subjected to whole-exome sequencing. The candidate variants were validated, and their pathogenicity was interpreted. Results FBN1 (NM_ 000138. 5) gene variants were found in all sevenpatients, including 5 previously reported variants [ c. 367T > C ( p. Cys123Arg), c. 2093C > T(p. Pro698Leu), c. 7532 G > A (p. Cys2511Tyr), c. 6815 A > G (p. Tyr2272Cys), (c. 7279T > C(p. Cys2427Arg)], 1 novel variant [ c. 316C > T ( p. Gln106Ter)], and 1 first reported variant in Chinese [c. 6354C> T (p. Ile2118 = )] . According to the ACMG guidelines, six variants of above were classified as pathogenic / likely pathogenic, and one variant was classified as a variant of uncertain significance. Conclusion The identification of novel pathogenic variants in the FBN1 gene expands the known mutational spectrum and provides insights into the genetic basis of MFS, which is crucial for clinical diagnosis and patient management. Related Articles | Metrics Select Effect of Linc279227 on Renal Injury in Diabetes Nephropathy Mice via PINK1 / Parkin Mediated Mitochondrial Autophagy #br# SHEN Qun, WANG Limin, DENG Wei, XIONG Wen, XIE Hongwu Journal of Medical Molecular Biology    2025, 22 (4): 319-324.   DOI: 10.3870/j.issn.1672-8009.2025.04.003 Abstract （198）      PDF （2780KB）（33）       Knowledge map    Save Objective To explore the effect and mechanism of TONCS _ 00279227(Linc279227) on renal injury in diabetes nephropathy mice. Methods Mice were divided into aControl group and a Model group. After successful modeling of db / db mice in the Model group, the mice kidney tissues were taken. qRT-PCR was used to detect the expression levels of Linc279227, PINK1, and Parkin in mice kidney tissues. Western blotting was used to detect the protein expression levels of LC3-Ⅱ , P62, PINK1, and Parkin in mice kidney tissues. Mouse renal podocyte MPC5 cells were divided into 3 groups: Vector group, Linc27922 group, and Linc27922 group. CCK8 and flow cytometry were used to detect cell proliferation and apoptosis. Western blotting was used to detect the expression levels of LC3-Ⅱ , P62, PINK1, and Parkin proteins in eachgroup of cells. Results Compared with those in the Control group, the expression levels of Linc279227 and P62 protein in the renal tissues of the model group mice were significantly upregulated (P< 0. 01), while the expression levels of PINK1 and Parkin mRNA and proteins and the LC3-Ⅱ protein were significantly downregulated (P < 0. 01) . Compared with those in the Vectorgroup, the mRNA and protein expression levels of PINK1 and Parkin and the protein expression level of LC3-Ⅱ in MPC5 cells of the Linc279227 group were significantly downregulated (P < 0. 01), and the expression level of P62 was significantly upregulated (P < 0. 01) . Compared with those inthe Linc279227 group, the LC3-Ⅱ expression level of MPC5 cells in the Linc27922 + FCCP group wasupregulated (P < 0. 01), the expression level of P62 was significantly downregulated (P < 0. 01), the cell proliferation ability was significantly increased (P<0. 05), and the cell apoptosis was significantly reduced (P < 0. 01) . Conclusion Linc279227 can mediate mitochondrial autophagy of nephropodocytes by regulating the PINK1 / Parkin pathway to affect renal injury in diabetes nephropathy mice. Related Articles | Metrics Select MCL1 Promotes Drug Resistance of Acute T Lymphoblastic Leukemia Cells to Venetoclax by Regulating GSK3β/ Wnt / β-Catenin Axis #br# MA Lina, HAO Jianping, ZHANG Rui, Dilinazi Abulaiti, ZHAO Fang, JIANG Ming Journal of Medical Molecular Biology    2025, 22 (4): 325-331.   DOI: 10.3870/j.issn.1672-8009.2025.04.004 Abstract （119）      PDF （3474KB）（41）       Knowledge map    Save Objective To investigate the molecular mechanism by which myeloid cell leukemiafactor 1 ( MCL1) promotes the resistance of acute T lymphoblastic leukemia ( T-ALL) cells tovenetoclax. Methods T-ALL parental cell line Jurkat and T-ALL venetoclax-resistant cell line Jurkat / VEN were cultured, and small interfering RNA targeting MCL1 (si-MCL1) and negative control (si-NC) were transfected into Jurkat / VEN cells. RT-qPCR and Western blotting were used to detect the expression level of MCL1 in transfected cells to verify the transfection effect. The expression levels of GSK3β, phosphorylated GSK3β ( p-GSK3β), β-catenin, c-Myc, and cyclin D1 were detected by Western blotting. Jurkat / VEN cells were divided into 4 groups: control group, siNC group, si-MCL1 group, si-MCL1 + CHIR-99021 group. The CCK-8 method was used to detect the survival rate of Jurkat / VEN cells in each group under different concentrations (0, 100, 200, 300, 400, 500 nmol / L) of venetoclax, the colony formation assay was used to detect the numberof colonies formed in each group, and the flow cytometry was used to detect the apoptosisrate. Results Compared with those in the Jurkat cells, the protein expression level of MCL1 in theJurkat / VEN cells was increased (P < 0. 05), the expression level of GSK3β was decreased (P <0. 05), and the expression levels of p-GSK3β, β-catenin, c-Myc and Cyclin D1 were increased(P < 0. 05) . Compared with those in the control group and si-NC group, the mRNA and proteinexpression levels of MCL1 were decreased in the si-MCL1 group (P < 0. 05), the expression levelof GSK3β was increased (P < 0. 05), and the expression levels of p-GSK3β, β-catenin, c-Mycand Cyclin D1 proteins were decreased (P< 0. 05) . Compared with those in the control group andsi-NC group, the survival rate after venetoclax treatment and the value of IC50 were decreased in thesi-MCL1 group (P< 0. 05), the number of colonies was decreased (P< 0. 05), and the apoptosisrate was increased (P< 0. 05) . Compared with those in the si-MCL1 group, the survival rate aftervenetoclax treatment and the value of IC50 were increased in the si-MCL1 + CHIR-99021 group (P<0. 05), the number of colonies was increased (P < 0. 05), and the apoptosis rate was decreased(P< 0. 05) . Conclusion Interference in MCL1 expression can reduce the drug resistance ofJurkat / VEN cells to venetoclax, which may be achieved by blocking the GSK-3β / Wnt / β-cateninsignaling axis. Related Articles | Metrics Select c-Myc / miR-27b-3p Promote Multiple Myeloma Cell Survival by Upregulating Bcl-2 #br# XUE Qin, TIAN Xinwei, WANG Jing, ZHENG Qili, Aibiba Abudula Journal of Medical Molecular Biology    2025, 22 (4): 332-338.   DOI: 10.3870/j.issn.1672-8009.2025.04.005 Abstract （110）      PDF （1893KB）（20）       Knowledge map    Save Objective To explore the molecular mechanisms of c-Myc / miR-27b-3p / Bcl-2 axison promoting multiple myeloma ( MM) cell survival. Methods The relative expression levels ofMM-related genes and microRNAs (miRNAs) were measured in human MM cell lines RPMI8226 and U266 cells by using qPCR analysis. TargetScan and dual-luciferase gene reporter assay were used to predict and verify the targeting relationship between miR-27b-3p and Bcl-2, respectively. The primary MM cells were isolated from 14 patients with MM recruited from the Fifth Affiliated Hospital of Xinjiang Medical University. The mRNA expression levels of c-Myc, Bcl-2, and the expression level of miR-27b-3p in primary MM cells were detected by qPCR. Pearson correlation analysis was used to analyze the relationship among their expression levels. Adenovirus vectors with c-Myc or Bcl-2 overexpression ( Bcl-2 OE, c-Myc OE), or miR-27b-3p inhibitor ( miR-27b-3p inhibitor) were constructed and transfected into the BMSCs. The expression levels of p-STAT3, STAT3,p-JAK2, and JAK2 in BMSCs were detected by Western blotting. Results Compared with those in the BMSCs, the mRNA expression levels of c-Myc and Bcl-2 were upregulated in the RPMI8226cells and the U266 cells (P < 0. 01), and miR-27b-3p was downregulated in the RPMI8226 cells and the U266 cells (P< 0. 01). Dual-luciferase gene reporter assay results showed that miR-27b-3p was directly targeted to the Bcl-2 3′-UTR. qPCR and Pearson correlation analysis showed that therelative expression levels of c-Myc mRNA and miR-27b-3p, miR-27b-3p and Bcl-2 mRNA werelinearly and negatively correlated (P< 0. 01), while the relative expression levels of c-Myc mRNA and Bcl-2 mRNA were linearly and positively correlated ( P < 0. 01). Compared with those in theBMSCs group, the expression levels of p-STAT3, STAT3, p-JAK2, and JAK2 in the BMSCs + cMyc OE group, the BMSCs + miR-27b-3p inhibitor group, and the BMSCs + Bcl-2 OE group wereall increased (P< 0. 05). Conclusion c-Myc upregulation and miR-27b-3p inhibition activated theBcl-2 to promote cell survival in MM. Related Articles | Metrics Select Effect and Mechanism of miR-200a-3p on Hypoxic-ischemic Brain Damage in Neonatal Rats #br# REN Hua, HAO Qiang, GUO Li, ZHENG Suhua, WEI Lei Journal of Medical Molecular Biology    2025, 22 (4): 339-345.   DOI: 10.3870/j.issn.1672-8009.2025.04.006 Abstract （101）      PDF （3700KB）（20）       Knowledge map    Save Objective To explore the effect of microRNA-200 a-3 p ( miR-200a-3p) on hypoxic-ischemic brain damage (HIBD) in neonatal rats. Methods Sixty neonatal SD rats were divided into 4 groups: sham operation group, HIBD group, miR-200a-3p antagomir group, and NCantagomir group, 15 cases in each group. The rat neonatal HIBD model was constructed. The expression level of miR-200a-3p in the hippocampus was detected by quantitative PCR. The nerve functionand brain water content were evaluated. The pathological changes and apoptosis of the hippocampal tissues were observed by HE staining and TUNEL staining. The levels of oxidative stress, inflammatory factors, and the expression levels of apoptosis-related proteins were detected by ELISA andWestern blotting. Results Compared with those in the sham operation group, the expression levelof miR-200a-3p in the hippocampus, the score of nerve function, the brain water content, the apoptosis rate of brain cells, the levels of MDA, IL-6, IL-1β, TNF-α and the expression level ofCleaved-Caspase-3 were increased (P < 0. 05), while the levels of SOD, CAT, Bcl-2 / Bax, BDNF and TrkB were decreased in the HIBD group (P < 0. 05) . Compared with those in the NC-antagomir group, the expression level of miR-200a-3p in the hippocampus, the score of nerve function, the brain water content, the apoptosis rate of brain cells, the levels of MDA, IL-6, IL-1β,TNF-α and the expression level of Cleaved-Caspase-3 were decreased (P < 0. 05), while the levels of SOD, CAT, Bcl-2 / Bax, BDNF and TrkB were increased in the miR-200a-3p antagomir group (P < 0. 05 ) . Conclusion InhibitingmiR-200a-3pcan reduce nerve injury in neonatal rats with HIBD, which may be related to the inhibition of apoptosis and oxidative stress, and the regulation of BDNF / TrkB pathway. Related Articles | Metrics Select Effect of miR-181c on Cardiopulmonary Function Rehabilitation in Mice Undergoing Lung Transplantation by Targeting MICU1 #br# Buaijier Aili, Mierguli Aimaite, LI Chunli, DUAN Pingxiu, LI Jinxian Journal of Medical Molecular Biology    2025, 22 (4): 346-353.   DOI: 10.3870/j.issn.1672-8009.2025.04.007 Abstract （107）      PDF （3319KB）（119）       Knowledge map    Save Objective To investigate how miR-181c influences cardiopulmonary recovery afterlung transplantation in mice by targeting mitochondrial calcium uniporter 1 (MICU1) . Methods Fifty-four adult male C57BL / 6 mice were randomly assigned to six groups (n = 9 each): Normalgroup, Lung Transplantation group, Lung Transplantation + inhibitor-NC group, Lung Transplantation + miR-181c-inhibitor group, Lung Transplantation + miR-181c-inhibitor + si-NC group, andLung Transplantation + miR-181c-inhibitor + si-MICU1 group. The Normal group underwent anesthesia and thoracotomy only; the other groups received autologous left lung orthotopic transplantation,followed by weekly tail-vein injections (0. 2 mL) of saline or 10 nmol / mL inhibitor / siRNA for 60days. qRT-PCR and Western blotting were use to detect miR-181c and MICU1 mRNA and protein expression levels. Dual-luciferase gene reporter assay was performed to verify the targeting relationship between miR-181c and MICU1. Pulmonary pathology was assessed by hematoxylin-eosin (HE) staining. Pulmonary function was assessed using a small animal pulmonary function test system [0. 15 s forced expiratory volume as a percentage of forced vital capacity ( FEV0. 15 / FVC), peak expiratory flow (PEF), maximum ventilation volume ( MVV), diffusing capacity of the lung for carbon monoxide ( DLCO), and residual volume ( RV)] . Cardiac function was detected using small animal ultrasound imaging technology [ left ventricular ejection fraction ( LVEF), left ventricular fractional shortening (LVFS), left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter ( LVESD), left ventricular end-diastolic volume ( LVEDV), and left ventricular end-systolic volume (LVESV)] . Results The expression level of miR-181c was elevated and that of MICU1 was reduced in the Lung transplantation group versus those in the Normalgroup (P< 0. 05), with a significant negative correlation (r = - 0. 378, P = 4. 21 × 10 - 4 ) . miR- 181c mimic suppressed MICU1-3′ UTR-WT luciferase activity ( P < 0. 05 ) but not 3′ UTRMUT. Inhibition of miR-181c expression restored MICU1 expression, and reduced lung lesions, and improved FEV0. 15 / FVC, PEF, MVV, DLCO, LVEF, LVFS, and decreased RV, LVESD, LVEDV, LVESV ( all P < 0. 05) . These gains were abolished by co-silencing MICU1 and miR-181c (P< 0. 05) . Conclusion miR-181c impairs cardiopulmonary recovery after lung transplantation bytargeting MICU1. miR-181c inhibition enhances post-transplant function. Related Articles | Metrics Select Effect of miR-107 and ITGA2 on Apoptosis of Pulmonary Artery Smooth Muscle Cells in Pulmonary Arterial Hypertension #br# WU Fengping, SHI Zongmin, ZHANG Yuanmei Journal of Medical Molecular Biology    2025, 22 (4): 354-360.   DOI: 10.3870/j.issn.1672-8009.2025.04.008 Abstract （100）      PDF （2600KB）（162）       Knowledge map    Save Objective: To investigate the effect of miR-107 and integrin alpha 2 (ITGA2) onpulmonary artery smooth muscle cells ( PASMCs) in pulmonary arterial hypertension ( PAH).Methods Pulmonary artery smooth muscle cells (PASMCs) were cultured under normal and hypoxic conditions. qRT-PCR was applied to detect the expression levels of miR-107 and ITGA2 in the cells. Flow cytometry was used to determine cell cycle and apoptosis. The targeting relationship between miR-107 and ITGA2 was verified by luciferase reporter gene assay. PASMCs were transfected with si-NC and si-miR-107 and cultured under hypoxic conditions, and were divided into the si-NC group and the si-miR-107 group. The expression levels of miR-107 and ITGA2, the cell cycle, and apoptosis were examined. Thirty C57BL / 6 mice were divided into 3 groups: control group, model group, and si-miR-107 treatment group, with the latter two groups injected with si-NC and si-miR- 107 after inducing a PAH model through hypoxia, respectively. The right ventricular hypertrophy in dex (RVHI), right ventricular systolic pressure ( RVSP), and mean pulmonary arterial pressure (mPAP) were measured. The expression levels of miR-107 and ITGA2, and phosphorylated histone H2AX (γH2AX) protein in the mouse lung tissues were detected by qRT-PCR and Western blotting. Results Compared with those of cells in the normal group, the expression level of miR-107 inthe hypoxic group cells was increased, the ITGA2 expression level was decreased, the proportion of cells in the G 1 phase was increased, the proportion of cells in the S phase was decreased, and the apoptosis rate was increased. miR-107 targeted ITGA2. Compared with those in the si-NC group, the expression level of miR-107 in the si-miR-107 group was decreased, the ITGA2 expression level was increased, the proportion of cells in the G1 phase was decreased, the proportion of cells in the S phase was increased, and the apoptosis rate was decreased. In the mice experiments, compared with those in the control group, the values of RVHI, RVSP, and mPAP, the expression level of miR-107 and γH2AX protein was increased, and the ITGA2 expression level was decreased in the model group. Compared with those in the model group, the values of RVHI, RVSP, and mPAP, the expression levels of miR-107 and γH2AX protein were decreased in the si-miR-107 treatmentgroup, while the expression level of ITGA2 was increased. Conclusion miR-107 affects PAH byinhibiting the cell cycle and promoting the apoptosis of PASMCs through ITGA2. Related Articles | Metrics Select Tanshinone Ⅱ A Regulates Proliferation, Invasion, and Migration of Colon Cancer SW480 Cells by Targeting miR-143 via MALAT1 #br# LI Peng, DU Rui, XIE Fuping, LI Jintao, WANG Jie Journal of Medical Molecular Biology    2025, 22 (4): 361-367.   DOI: 10.3870/j.issn.1672-8009.2025.04.009 Abstract （91）      PDF （4820KB）（17）       Knowledge map    Save Objective To investigate the effect of tanshinone Ⅱ A on proliferation, invasionand migration of colon cancer SW480 cells by targeting miR-143 via metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) . Methods SW480 cells were treated with 0, 10, 20, and40 μmol / L of tanshinone Ⅱ A, and were randomly divided into 4 groups: Control group, tanshinone Ⅱ A low-, medium-, and high-dose groups. CCK8 assay was used to detect cellproliferation. Wound-healing and Transwell assay were used to detect the number of migrated and invaded cells. The expression levels of MALAT1 and miR-143 mRNA were detected by RT-PCR. Theluciferase gene reporter assay was used to verify the targeting relationship between MALAT1 andmiR-143. SW480 cells treated with tanshinone Ⅱ A (40 μmol / L) were transfected with pcDNA MALAT1 and miR-143 mimic separately or combined, and were randomly divided into 5 groups:Control group, PCDNA 3. 1 group, pcDNA-MALAT1 group, MALAT1 + mimic NC group, and MALAT1 + miR-143 mimic group. The proliferation, invasion, and migration of cells in the abovegroups were detected. Results Compared with those in the Control group, the cell proliferation,number of invaded cells, wound-healing rate, and MALAT1 mRNA expression level in the tanshinone Ⅱ A medium-dose and high-dose groups were significantly decreased ( P < 0. 05), and the miR-143 mRNA expression level was significantly increased (P< 0. 05) . MALAT1 has a targetingrelationship with miR-143. Compared with those in the pcDNA-MALAT1 group, the cell proliferation, number of invaded cells, and wound-healing rate in the MALAT1 + miR-143 mimic groupwere significantly decreased (P< 0. 05) . Conclusion Tanshinone Ⅱ A exerts its anti-colon cancer effect through theMALAT1 / miR-143 axis. Related Articles | Metrics Select Effect of circCSE1L on the Metastatic Activity of Non-small Cell Lung Cancer NCI-H1299 Cells by Regulating MiR-16-5p #br# LIU Ying, ZHANG Yong, LI Qiubo, HUANG Nian Journal of Medical Molecular Biology    2025, 22 (4): 368-373.   DOI: 10.3870/j.issn.1672-8009.2025.04.010 Abstract （118）      PDF （4200KB）（26）       Knowledge map    Save Objective To investigate the effect of circCSE1L on the metastatic activity of nonsmall cell lung cancer NCI-H1299 cells by regulating miR-16-5p. Methods The expression level ofmiR-16-5p and circCSE1L in cancer tissues and adjacent tissues of patients with non-small cell lung cancer was analyzed by real-time quantitative PCR. NCI-H1299 cells were divided into 4 groups: si NC group, si CSE1L group, miR NC group, and miR-16-5p mimic group. The proliferation activity of cells was analyzed by MTT assay. The invasion and migration abilities of cells were analyzed by Transwell assay and wound-healing assay. The apoptosis rate of cells was analyzed by flow cytometry. Luciferase reporter gene assay was used to analyze the targeting relationship between circCSE1L and miR-16-5p in NCI-H1299 cells. Results Compared with those in the adjacent tissues, circCSE1L was highly expressed in the NSCLC tissues, while miR-16-5p was lowly expressed in the NSCLC tissues. Compared with those in the si NC group, the cell proliferation activity, invasion and migration abilities in the si CSE1L group were decreased, and the apoptosis rate was increased. Compared with those in the miR NC group, the cell proliferation activity, invasion and migration abilities of in the miR-16-5p mimic group were decreased, and the apoptosis rate was increased. The luciferase activity was decreased after transfection with miR-16-5p mimic in the CSE1LWT group compared with that in the miR NC group. Conclusion circCSE1L was highly expressedin NSCLC, while miR-16-5p was lowly expressed. circCSE1L affects the proliferation, migration, and invasion of non-small cell lung cancer NCI-H1299 cells by inhibiting the expression of miR-16- 5p, and promotes the apoptosis of non-small cell lung cancer cells. Related Articles | Metrics Select Predictive Value of Serum ZO-1, Occludin, Claudin-1 Combined with APACHEⅡ Score in Hypertriglyceridemia-induced Severe Acute Pancreatitis Complicated with Acute Kidney Injury #br# XU Jingjing, CHEN Jiaping, XU Lingqi, LIN Ying, HUANG Hao Journal of Medical Molecular Biology    2025, 22 (4): 374-378.   DOI: 10.3870/j.issn.1672-8009.2025.04.011 Abstract （126）      PDF （878KB）（33）       Knowledge map    Save Objective To investigate the predictive value of serum tight junction protein zonulaoccludens 1 (ZO-1), occludin, claudin-1, combined with acute physiology and chronic health evaluation Ⅱ ( APACHE Ⅱ ) score on hypertriglyceridemia-induced severe acute pancreatitis(HTG-SAP) complicated with acute kidney injury (AKI) . Methods A total of 96 patients withHTG-SAP admitted from January 2021 to March 2024 were retrospectively studied and divided intoAKI group (n = 38 ) and non-AKI group ( n = 58 ) according to whether they had concurrentAKI. Differences in clinical data and serum ZO-1, occludin, and claudin-1 levels were compared between the two groups. Factors with statistically significant differences were screened as independent variables for logistic regression analysis, and a prediction model was constructed. The predictive value of each index on HTG-SAP complicated AKI was analyzed by the receiver operating characteristiccurve. Results The APACHEⅡ score, systemic inflammatory response syndrome score, triglyceride, serum creatinine and blood urea nitrogen levels in the AKI group were higher than those in thenon-AKI group, and serum ZO-1, occludin, and claudin-1 levels were lower than those in the nonAKI group, the differences were statistically significant ( P < 0. 05) . Logistic regression analysisshowed that the increased of APACHEⅡ score (OR = 1. 781, 95 % CI: 1. 065-2. 981), and thedecreased levels of serum ZO-1 (0. 956, 95 % CI: 0. 918-0. 995), occludin (0. 967, 95 % CI:0. 941-0. 995) and claudin-1 ( 0. 193, 95 % CI: 0. 049-0. 752 ) were risk factors for AKI inHTG-SAP patients (P< 0. 05) . The area under the curve of APACHEⅡ score and serum ZO-1, occludin, claudin-1 alone and combined models in predicting AKI in HTG-SAP patients were 0. 821(95 % CI: 0. 740-0. 902), 0. 852 (95 % CI: 0. 740-0. 902), 0. 877 (95 % CI: 0. 807-0. 947),0. 936 (95 % CI: 0. 891-0. 981), 0. 998 (95 % CI: 0. 993-1. 000), respectively. Conclusion  The decrease of serum tight junction proteins ZO-1, occludin, and claudin-1 and the increase of APACHEⅡ score are the risk factors of AKI in HTG-SAP patients. Establishing a prediction model according to these four indexes has good value in predicting AKI in HTG-SAP patients. Related Articles | Metrics Select Preventive Health Examination of Employees: Examination of Salmonella and Shigella by Quantitative Real-time PCR #br# LI Ying, LI Ruonan, SUN Nan Journal of Medical Molecular Biology    2025, 22 (4): 379-382.   DOI: 10.3870/j.issn.1672-8009.2025.04.012 Abstract （114）      PDF （955KB）（9）       Knowledge map    Save Objective To investigate the use of quantitative real-time PCR as an alternative tothe screening plate culture method for the detection of salmonella and shigella in pre-employmenthealth examinations, comparing the two methods in terms of detection rate, cost, and duration oftesting. Methods Compare the screening test results of salmonella and shigella detection using thebacterial screening plate culture method in 10 100 cases in 2023 with the screening test results ofsalmonella and shigella detection using the quantitative real-time PCR method in 9 842 cases in2024. Results Quantitative real-time PCR method demonstrated a high level of screening power(91 / 9 842 in 2024 vs. 0 / 10 100 in 2023) with a lower total cost (4. 4 yuan / sample in 2004 vs. 6. 9 yuan / sample in 2023) . In addition, quantitative real-time PCR can be implemented without increasing the testing duration and is easy to carry out. Conclusion Quantitative real-time PCR can be usedas a screening test for salmonella and shigella detection in pre-employment health examinations. Related Articles | Metrics Select Causal Effects and Immune Cell Mediators between Gut Microbiota and Risk of Acute Glomerulonephritis: A Mendelian Randomization Study #br# LUO Jiamei, GUO Jing, CHEN Shasha, ZHANG Yong Journal of Medical Molecular Biology    2025, 22 (4): 383-391.   DOI: 10.3870/j.issn.1672-8009.2025.04.013 Abstract （99）      PDF （3160KB）（37）       Knowledge map    Save Objective To investigate whether immune cells mediate the causal relationship between the gut microbiota and acute glomerulonephritis ( AGN) through Mendelian randomization(MR) analysis. Methods A two-sample bidirectional MR approach was employed to assess thecausal effect of gut microbiota on AGN. Additionally, a two-step MR strategy was applied to identify potential immune cells mediating this effect. Data from genome-wide association studies ( GWAS) encompassing 473 gut microbial taxa, 731 immune cell traits, and AGN outcomes were included. The primary analysis utilized inverse variance weighted ( IVW) randomization, supported by MR-Egger, weighted median, simple mode, and weighted mode analyses. Sensitivity checks included Cochran’s Q test, MR-PRESSO test, MR-Egger regression intercept, and leave-one-out analysis. Results Fourteen gut microbial taxa and 27 immune cell types were identified as causallyassociated with AGN. Mediation analysis highlighted that 12 immune cell types mediated the relationship between 9 gut microbial taxa and AGN risk. Notably, Barnesiellaceae and Holdemania werefound to promote AGN risk through 4 immune cell mediators. Additionally, BAFF-R on IgD + CD38 - unsw mem (unswitched memory B cells) mediated the protective effect of Lactobacillus B on AGN, with a mediation effect of 2. 9 % and a mediating proportion of - 7. 50 % . Hydrogenoanaerobacterium exerted its protective effect on AGN risk via HSC AC and CD25 on CD4 Treg, mediating proportions of 10. 60 % and 7. 50 % , respectively. Conclusion This study delineates acomplex network involving gut microbiota, immune cells, and AGN, reflecting multifaceted pathophysiological interactions. The identified causal links and mediating pathways underscore potential therapeutic targets, providing a theoretical foundation for interventions aimed at modulating gut microbiota and immune responses to manage AGN. Related Articles | Metrics Select Research Progress on Regulatory T cells in Hepatic Inflammatory Injury #br# ZHANG Yuting, LIU Liangming Journal of Medical Molecular Biology    2025, 22 (4): 392-398.   DOI: 10.3870/j.issn.1672-8009.2025.04.014 Abstract （106）      PDF （2506KB）（41）       Knowledge map    Save Regulatory T cells ( Tregs) play multifaceted roles in hepatic inflammatory injury. On one hand, Tregs can migrate to inflamed hepatic tissues via chemokine-mediated chemotaxis, exerting immunosuppressive functions and promoting tissue repair. On the other hand, during the fibrotic process induced by inflammatory injury, the interactions between Tregs and other immune cells can counteract fibrogenesis. This review focuses on the classification and functions of Tregs, their specific roles in hepatic inflammatory injury diseases, and the underlying mechanisms mediating their actions in hepatic inflammation and injury, to elucidate the intricate mechanisms by which Tregs modulate hepatic inflammatory injury and further clarify the complexity of hepatic immune cell interactions. Related Articles | Metrics Select Effect of High-risk Human Papillomavirus L1 and L2 Proteins on Autophagy in Cervical Cancer #br# GAO Xun, WANG Zhilian Journal of Medical Molecular Biology    2025, 22 (4): 399-402.   DOI: 10.3870/j.issn.1672-8009.2025.04.015 Abstract （92）      PDF （712KB）（23）       Knowledge map    Save Autophagy is a self-consumption mechanism used by cells to maintain homeostasis inthe body. Some findings suggest that high-risk human papillomavirus (HR-HPV) promotes cervical carcinogenesis by acting on host cell autophagy. HR-HPV can integrate the viral genome into the host DNA, which in turn infects the host cell. HR-HPV L1 and L2 proteins assist viral entry into cells and inhibit the autophagic process by activating the PI3K / AKT / mTOR signalling pathway through interactions with cell-surface receptors on the membrane of the target cell, resulting in the uninterrupted transport of viral particles into the cell. At the end stage of viral infection, HR-HPV L1 and L2 proteins are expressed in the cytoplasm and translocate to the nucleus, assisting viral evasion of immune surveillance by affecting autophagy. Although HPV prophylactic vaccines against HR-HPV L1 and L2 proteins are available, clarifying the specific regulation of autophagy in cervical cancer by HR-HPV L1 and L2 proteins may expand new ideas for cervical cancer prevention and treatment. Related Articles | Metrics Select Research Progress on Resistance Mechanisms of Helicobacter pylori to Clarithromycin #br# WANG Yinfeng, CHEN Changxi, LI Hongliang Journal of Medical Molecular Biology    2025, 22 (4): 403-408.   DOI: 10.3870/j.issn.1672-8009.2025.04.016 Abstract （129）      PDF （724KB）（7）       Knowledge map    Save Helicobacter pylori (HP) is a major pathogen responsible for various gastrointestinaldiseases, and its eradication plays a critical role in preventing gastric cancer. The resistance of HP to clarithromycin has become a key issue affecting its eradication. This article reviews the main molecular mechanisms of HP resistance to clarithromycin, aiming to provide a theoretical foundation for optimizing treatment strategies and future antimicrobial research. Related Articles | Metrics Select Influenza Virus Induces Degradation of Interferon Signaling Pathway Proteins to Promote Its Own Proliferation #br# HE Chenmei, FAN Shao, XIA Chuan Journal of Medical Molecular Biology    2025, 22 (4): 409-414.   DOI: 10.3870/j.issn.1672-8009.2025.04.017 Abstract （111）      PDF （3484KB）（22）       Knowledge map    Save Influenza, also known as the flu, is an acute respiratory infectious disease causedby the influenza virus. It has a high incidence rate and can lead to patient mortality. To create a suitable environment for replication and proliferation, the influenza virus engages in complex interactions with the host, including the regulation of host cell gene expression and various signaling pathways by the virus. The type I interferon signaling pathway, as the first line of defense against viral infections, is an important component of the host’s antiviral innate immunity. Meanwhile, type Ⅱ and type Ⅲ interferon systems also influence viral replication through different mechanisms. Literature reports that influenza virus can induce degradation of related cellular proteins to evade the host’s antiviral immune response. This article focuses on the regulation of the interferon system by influenza virus, discussing the molecular mechanisms and biological significance of how the virus promotes ubiquitination and degradation of proteins related to typeⅠ , Ⅱ , and Ⅲ interferon pathways. Understanding how influenza virus antagonizes interferon-mediated antiviral responses is conducive to the development of new anti-influenza therapies by targeting host factors. Related Articles | Metrics Select Construction and Functional Validation of a Novel Biological Activity Detection System for BMP-2#br# FU Yueyang, #, XIA Zhiyi#, YANG Jianxun, WANG Biru, ZHENG RuiΔ, YAN BoΔ Journal of Medical Molecular Biology    2025, 22 (5): 415-422.   DOI: 10.3870/j.issn.1672-8009.2025.05.001 Abstract （138）      PDF （1342KB）（87）       Knowledge map    Save Objective To develope a novel BMP-2 bioactivity detection system based on a dual-luciferase reporter gene stably transfected cell line (C2C12BBDE) to address the issues of low sensitivity, time-consuming procedures in traditional alkaline phosphatase ( ALP) activity assays, and cumbersome operational workflows in real-time fluorescent quantitative polymerase chain reaction(qRT-PCR ) methods. Methods This system integrates a BMP-2 responsive promoter driving NanoLuc luciferase (NLuc) expression with constitutively expressed Firefly luciferase ( Fluc) as an internal control via lentiviral transduction. Potential promoter interference was mitigated through strategic design of an inverse transcription unit and PolyA sequence insertion. Results This novel system achieved a dynamic detection range of 0-30 ng / mL, matching the sensitivity of qRT-PCR while demonstrating a statistically significant improvement over the ALP assay. Furthermore, the assay cycle was markedly reduced to 16 hours, representing an efficiency enhancement exceeding 700 % relative to the ALP method. Critically, the workflow is streamlined, obviating the need for complex RNA extraction and reverse transcription steps inherent in qRT-PCR. Conclusion The successful establishment of this system not only furnishes a standardized, high-throughput tool for BMP-2 bioactivity assessment but also provides a modular, adaptable technical paradigm for the development of bioactivity assays for other growth factors. This advancement holds substantial translational potential, significantly contributing to the rational development and clinical implementation of bone regenerative therapeutics. Related Articles | Metrics Select Effect of Schisandra chinensis Lignans on Neuronal Apoptosis and Mitochondrial Damage in Sleep Deprivation Model Rats #br# ZHAO Yi, LI Hua, HU Xia, CHANG Haixia Journal of Medical Molecular Biology    2025, 22 (5): 423-429.   DOI: 10.3870/j.issn.1672-8009.2025.05.002 Abstract （712）      PDF （5850KB）（46）       Knowledge map    Save Objective To explore the molecular mechanism by which Schisandra chinensis lignans (SCL) improve neuronal apoptosis and mitochondrial damage in the sleep deprivation (SD) model rats. Methods Forty-eight rats were divided into 6 groups: Control group, SD group, modafinil ( MOD) group ( positive control), and SCL treatment groups at different concentrations. The Morris water maze and Y-maze tests were used to assess the escape latency and behavioral accuracy of rats in each group, respectively. HE staining was used to detect hippocampal tissue pathological damage in rats, and TUNEL staining was used to detect cell apoptosis. JC-1 staining and ELISA were used to detect the levels of mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) in rats’brain tissues and cells. An in vitro neuronal damage model was established using the ROS inducer 2, 3-dimethoxy-1, 4-naphthoquinone (DMNQ) to stimulate HT-22 cells. CCK-8 was used to measure cell viability. Western blotting was used to detect the expression levels of TLR4, MyD88, and p-NF-κB P65 in cells. Results Compared with those in the Control group, the escape latency of SD rats increased, and behavioral accuracy decreased. In contrast, rats treated with Mod or SCL showed reduced escape latency and increased behavioral accuracy (all P<0.05). Additionally, compared with rats in the Control group, rats in the SD group exhibited significant hippocampal tissue pathological damage, increased cell apoptosis, decreased MMP levels, and increased ROS levels. Mod or SCL intervention improved hippocampal tissue damage and cell apoptosis and reduced neuronal mitochondrial damage in SD rats (all P< 0. 05). Cellular experimental results showed that HT-22 cells in the DMNQ group had reduced viability, increased apoptosis, and increased mitochondrial damage and ROS levels when compared with those in the Control group. Mod or SCL treatment significantly improved the DMNQ-induced HT-22 cell damage. Moreover, compared with those in the Control group, the protein expression levels of TLR4, MyD88, and pNF-κB P65 in the DMNQ group cells were elevated, and Mod or SCL intervention significantly suppressed the levels of TLR4, MyD88, and p-NF-κB P65 in DMNQ-treated HT-22 cells. Conclusion SCL improves neuronal apoptosis and mitochondrial damage in SD rats by inhibiting the activation of the TLR4-MyD88-NF-κB pathway. Related Articles | Metrics Select Clinical Significance of EGFR Expression and Amplification in Tongue Squamous Cell Carcinoma #br# WANG Yuanyuan, ZHAO Xiaoni, YANG Zhe, ZHANG Jiaojiao, XIA Nina, LI Xiaofeng, LIU Xi, WEI Xiaoyun Journal of Medical Molecular Biology    2025, 22 (5): 430-434.   DOI: 10.3870/j.issn.1672-8009.2025.05.003 Abstract （104）      PDF （7412KB）（38）       Knowledge map    Save Objective To explore the clinical significance of EGFR expression and amplification in tongue squamous cell carcinoma. Methods Detection of EGFR using immunohistochemistry and FISH was conducted in 34 cases of tongue squamous cell carcinoma and their adjacent tissues, along with one case of pseudoepitheliomatous hyperplasia of the tongue in tissue chips. Results The expression and amplification rates of EGFR in tongue squamous cell carcinoma were higher than those in adjacent normal tissues. Specifically, the expression rate of EGFR in cancer tissues was 63. 6 % (21 out of 33 samples), while in normal tissues, it was 0 % (0 out of 33 samples). Regarding amplification, the rate in cancer tissues was 5. 9 % (2 out of 33 samples), whereas it remained at 0 % (0 out of 33 samples) in normal tissues. EGFR expression was not associated with age, gender, tissue grading, or clinical stage, but it was associated with lymph node metastasis. Conclusion: Detection of EGFR is important for differentiating tongue squamous cell carcinoma in clinical pathology. The overexpression of EGFR protein is partially due to an increase in copy number, and an elevated level of EGFR indicates a poor clinical prognosis. Related Articles | Metrics Select Effect of Overexpression of miR-193b-5p on Autophagy to Reverse Cisplatin Chemotherapy Resistance in Cervical Cancer Cells #br# Reziwanguli Yuemaier, Maimaiti Simayi , ZHANG Xiaoling, Dilinuer Anwaier, ZHOU Ling Journal of Medical Molecular Biology    2025, 22 (5): 435-441.   DOI: 10.3870/j.issn.1672-8009.2025.05.004 Abstract （96）      PDF （3696KB）（22）       Knowledge map    Save Objective To investigate the effect and mechanism of overexpression of microRNA-193b-5p ( miR-193b-5p) on cisplatin ( DDP) -resistant cell line SiHa / DDP in human cervicalcancer. Methods Human cervical cancer cell line ( SiHa) and its cisplatin-resistant cell line( SiHa / DDP) were cultured. The survival rates of the two cell lines treated with DDP (5, 10, 15, 20, 25, 30 μmol / L) were detected by MTT assay, and the half inhibitory concentration ( IC50 ) value was determined. Cells were divided into 4 groups: SiHa group, SiHa / DDP group, mimics NC group ( SiHa / DDP cells transfected with mimics NC), miR-193b-5p mimics group ( SiHa / DDP cells transfected with miR-193b-5p mimics). The expression level of miR-193b-5p was detected by RT-qPCR. Cells were then treated with DDP, and the cell survival rate and apoptosis rate were detected by the MTT method and flow cytometry. The expression of microtubule-associated protein 1 light chain 3 B (LC3B) was detected by cell immunofluorescence staining, and the protein expression levels of LC3Ⅱ / LC3Ⅰ , Beclin-1, and P62 were detected by Western blotting. Results Thesurvival rate of SiHa / DDP cells was higher than that of the SiHa cells when treated with DDP at thesame concentration (P< 0. 05), and the IC50 value of cells was significantly increased (P< 0. 05).The relative expression level of miR-193b-5p in the SiHa / DDP cells was significantly downregulated(P< 0. 05). The relative expression level of miR-193b-5p in the miR-193b-5p mimics group was higher than that in the control group and mimics NC group (P< 0. 05). Compared with those in theSiHa / DDP group and the mimics NC group, the survival rate of SiHa / DDP cells in the miR-193b-5p mimics group was significantly decreased, the apoptosis rate was significantly increased ( P <0. 05), the fluorescence intensity of LC3B in cells was significantly weakened, the LC3Ⅱ / LC3Ⅰratio and the relative expression level of Beclin-1 protein were significantly downregulated ( P <0. 05), and the relative expression level of P62 protein was significantly upregulated (P < 0. 05).Conclusion The expression level of miR-193b-5p was decreased in the cisplatin-resistant cell lineSiHa / DDP of human cervical cancer. Its overexpression could reverse the resistance of SiHa / DDPcells to DDP, which may be related to its inhibition of cell autophagy. Related Articles | Metrics Select Effect of Lactic Acid Metabolism Genes on Prognosis of Lung Squamous Cell Carcinoma and Immune Microenvironment Based on Bioinformatics Analysis #br# CHEN Shengze, TANG Shishuai, ZHOU Mei, JIN Yang, XU Juanjuan Journal of Medical Molecular Biology    2025, 22 (5): 442-451.   DOI: 10.3870/j.issn.1672-8009.2025.05.005 Abstract （116）      PDF （13917KB）（19）       Knowledge map    Save Objective To screen out differentially expressed lactic acid metabolism genes inlung squamous cell carcinoma (LUSC), and to investigate their influence on LUSC prognosis andimmune microenvironment through bioinformatics analysis. Methods RNA sequencing and clinicaldata were obtained from public databases. Differentially expressed lactic acid metabolism genes in LUSC and normal tissues were identified by integrated bioinformatics analysis. Univariate Cox, LASSO and multivariate Cox regression analyses were applied to screen out survival-associated lactic acid metabolism genes. CIBERSORT was used to evaluate the relationship between gene expression atlas and immune cell infiltration in patients of different risk groups. Kaplan-Meier (KM) survival analysis and receiver operating characteristics ( ROC) were used to verify the predictive power of the model in an internal training cohort and an external validation cohort, respectively. Risk groups and clinical information were combined to produce a nomogram to predict the survival time of LUSC patients. Results A total of 34 survival-associated lactic acid metabolism genes were successfullyscreened out, and prognosis models were constructed based on these genes. According to this model, LUSC patients were divided into a high-risk group and a low-risk group. Resting CD4 + memoryT cells ( P = 0. 001), activated CD4 + memory T cells ( P < 0. 001), resting NK cells ( P =0. 03), monocytes (P = 0. 01), M0 macrophages (P = 0. 009), activated dendritic cells (P <0. 001), active mast cells (P = 0. 04) and neutrophils (P< 0. 001) in LUSC immune microenvironment were associated with risk groups. KM survival analysis showed that the total survival time ofthe low-risk group was significantly longer than that of the high-risk group (P< 0. 001). The areasunder the ROC curve (AUC) of LUSC patients at 1, 3 and 5 years were all larger than 0. 7. Aftercombining risk groups and clinical information, a nomogram was obtained that could predict the survival rate of LUSC patients at 1, 3 and 5 years, and the correction curve showed a good predictionaccuracy. Conclusion LUSC prognosis model and its risk groups constructed by 34 lactic acid metabolism genes can be used to evaluate the immune microenvironment and the survival rate of LUSCpatients at 1, 3 and 5 years. Related Articles | Metrics Select Identification of EPDR1 as Prognostic Biomarker of Gastric Cancer and Its Effect on Invasion and Migration of Gastric Cancer Cells #br# LIANG Chengxi, YANG Chaogang, XIONG Bin, Journal of Medical Molecular Biology    2025, 22 (5): 452-461.   DOI: 10.3870/j.issn.1672-8009.2025.05.006 Abstract （88）      PDF （15595KB）（13）       Knowledge map    Save Objective To analyze the expression level of recombinant ependymin-related protein 1 (EPDR1) in gastric cancer ( GC) and its relationship with the prognosis of GC patients,and to further explore the effect of EPDR1 on the invasive and migrative abilities of GC cells and itspotential mechanism. Methods The expression levels of EPDR1 in gastric cancer tissues and adjacent non-cancerous tissues from the GSE62254 dataset of the GEO database and TCGA-GTEx were analyzed, and their associations with clinicopathological characteristics and prognosis of corresponding patients were investigated. Gene set enrichment analysis (GSEA) was used to explore the signaling pathways that EPDR1 might regulate in GC. The effects of EPDR1 on the migration and invasion of GC cells and its potential mechanism were investigated by RT-qPCR, Western blotting, immunofluorescence, and Transwell assay. Results Bioinformatics analysis showed that EPDR1 was significantly overexpressed in both the primary and peritoneal metastases of GC, and its high expression was closely related to poor disease-free survival and overall survival of GC patients. GSEA analysis indicated that EPDR1 may participate in the occurrence and development of GC by activating theWnt / β-catenin signaling pathway. In vitro cell experiments showed that overexpression of EPDR1 enhanced the migrative and invasive abilities of GC cells, and activated the Wnt / β-catenin pathway topromote the up-regulation of CTNNB1 protein and endonuclear translocation. Conclusion EPDR1is highly expressed in GC, which is closely related to the invasion, migration, and poor prognosis of GC, and can be used as a prognostic biomarker and potential therapeutic target for GC. Related Articles | Metrics Select Effect of lncRNA ANRIL on Invasion and Stem Cell-like Characteristics of Ovarian Cancer Cells Skov-3 by Targeting miR-324-5p #br# ZHU Beibei, JIANG Yanli, GUO Min, DU Zhuo Journal of Medical Molecular Biology    2025, 22 (5): 462-468.   DOI: 10.3870/j.issn.1672-8009.2025.05.007 Abstract （92）      PDF （3303KB）（17）       Knowledge map    Save Objective To elucidate the molecular mechanism of lncRNA ANRIL in regulating the invasion and stem cell-like characteristics of ovarian cancer, and to analyze its dual role in mediating chemotherapy resistance and tumor recurrence. Methods ANRIL stable knockdown SKOV-3cell model was established (Control group, shRNA-NC group, ANRIL-shRNA1 group). The ability of cell invasion and metastasis was evaluated by Transwell assay, wound-healing assay, and the expression of VEGF and Fibronectin. The characteristics of stem cells were analyzed by tumor sphere formation assay combined with stem-cell marker CD44 / SOX2 / OCT4 detection. The targeting interaction between ANRIL-shRNA1 and miR-324-5p was verified by dual luciferase reporter assay. A functional recovery experiment ( ANRIL-shRNA1 + miR-324-5p inhibitor co-transfection group) was designed to clarify the mediating effect of miR-324-5p on the regulation of VEGF and CD44 by ANRIL-shRNA1. Results  ANRIL knockdown decreased the invasion and migration ability of SKOV-3cells, and the expression levels of VEGF and Fibronectin were significantly down-regulated. At the same time, the number of spheres was decreased, and the expression levels of CD44, SOX2, and OCT4 were decreased significantly compared with those in the control group. Dual luciferase assay confirmed that ANRIL directly binded to miR-324-5p. The inhibition of miR-324-5p could reverse the inhibitory effect of ANRIL knockdown on VEGF and CD44. Conclusion LncRNA ANRIL can promote cell invasion and help maintain the characteristics of tumor stem cells by targeting miR-324-5p. Related Articles | Metrics Select Sodium Butyrate Improves Acute Kidney Injury in Sepsis Through PI3K / AKT / Bax Pathway #br# WANG Boqing, LI Yan, YANG Jian, LUO Bin Journal of Medical Molecular Biology    2025, 22 (5): 469-475.   DOI: 10.3870/j.issn.1672-8009.2025.05.008 Abstract （96）      PDF （8985KB）（17）       Knowledge map    Save Objective To explore the effect and mechanism of sodium butyrate (NaB) on acute kidney injury (AKI) in mice with sepsis. Methods A sepsis AKI model was prepared in 30mice and randomly divided into 3 groups: model group, NaB low-dose ( NaB-L) group, NaB high-dose (NaB-H) group, with 10 mice in each group. Another 10 mice were taken as the Sham group. HE staining was used to observe the morphological changes in the kidneys of mice. Automatic biochemical analyzer was used to detect the levels of serum creatinine (Scr) and blood urea nitrogen (BUN). The chemiluminescence method was used to determine the levels of serum kidney injury molecule-1 (KIM-1). The ELISA method was used to determine the levels of inflammatory factors such as interleukin ( IL) -1β, IL-6, and tumor necrosis factor-α ( TNF-α) in renal tissues of mice. TUNEL staining was used to observe the apoptosis in renal tissue cells of mice. Western blotting and immunohistochemical staining were used to detect the expression of proteins related to the phosphatidylinositol 3-kinase ( PI3K ) / protein kinase B ( AKT) / B cell lymphoma-2 protein(Bcl) associated X protein (Bax) pathway in renal tissues of mice in each group. Results Compared with the Sham group, the model group showed swollen, detached, and necrotic renal tubular epithelial cells, and interstitial hemorrhage accompanied by obvious inflammatory cell infiltration, and glomerular expansion or atrophy. The renal injury score, the levels of Scr, BUN and KIM-1were increased in the model group (P< 0. 05), the levels of IL-1β, IL-6 and TNF-α in renal tissues were increased ( P < 0. 05), the proportion of TUNEL-positive cells was increased ( P <0. 05), the expression of p-PI3K, p-AKT and Bcl-2 were decreased (P< 0. 05), and the expression of Bax was increased (P< 0. 05). Compared with those in the model group, the lesions of renaltubular, interstitial and glomerular in mice in the NaB-L and NaB-H groups were alleviated, the renal injury score, the levels of Scr, BUN and KIM-1 were reduced (P < 0. 05), the levels of IL-1β, IL-6 and TNF-α in renal tissues were reduced (P< 0. 05), the proportion of TUNEL-positivecells was reduced ( P < 0. 05), and the expression of p-PI3K, p-AKT and Bcl-2 were increased(P< 0. 05), and the expression of Bax was decreased (P< 0. 05). Conclusion NaB can improverenal injury in septic mice, and its mechanism may be related to the activation of PI3K / Akt signaling pathway and the inhibition of Bax expression. Related Articles | Metrics Select Application of Serum IP-10, IL-2, MCP-1 and INF-γ Level in Diagnosis of Active Pulmonary Tuberculosis #br# WANG Bo, HAN Wei Journal of Medical Molecular Biology    2025, 22 (5): 476-427.   DOI: 10.3870/j.issn.1672-8009.2025.05.009 Abstract （76）      PDF （1180KB）（23）       Knowledge map    Save Objective To explore the application of serum interferon-gamma-induced protein10 (IP-10), interleukin-2 (IL-2), monocyte chemoattractant protein-1 ( MCP-1), and interferon-gamma (INF-γ) in the diagnosis of active tuberculosis (ATB). Methods The clinical data of110 ATB patients who visited Hongya County Traditional Chinese Medicine Hospital from November2023 to November 2024 were retrospectively analyzed as the observation group. Another 90 patientswith other lung diseases and 60 healthy individuals undergoing physical examinations during thesame period were selected as the lung disease group and the control group, respectively. The levelsof serum IP-10, IL-2, MCP-1 and INF-γ in the three groups were compared. The relationship between IP-10, IL-2, MCP-1, INF-γ and ATB was analyzed, and the receiver operating characteristic (ROC) curve was drawn to explore the diagnostic value of IP-10, IL-2, MCP-1, and INF-γfor ATB. Results The levels of IP-10, IL-2, MCP-1, and INF-γ in the observation group werehigher than those in the lung disease group and the control group (P< 0. 05); the levels of IP-10,IL-2, MCP-1, and INF-γ in the lung disease group were higher than those in the control group(P< 0. 05). ROC curve analysis showed that the combined diagnosis of ATB with IP-10, IL-2, MCP-1, and INF-γ (AUC: 0. 813, 95 % CI: 0. 784-0. 842) was superior to the single indicators of IP-10 ( AUC: 0. 663, 95 % CI: 0. 645-0. 681), IL-2 ( AUC: 0. 627, 95 % CI: 0. 611- 0. 643), MCP-1 (AUC: 0. 721, 95 % CI: 0. 685-0. 757), and INF-γ ( AUC: 0. 734, 95 % CI: 0. 692-0. 776) ( P < 0. 05). Logistic analysis revealed that elevated IP-10 ( OR: 3. 435, 95 % CI: 1. 874-4. 996 ), elevated IL-2 ( OR: 1. 314, 95 % CI: 1. 264-6. 178 ), elevated MCP-1 (OR: 3. 691, 95 % CI: 2. 521-5. 561), and elevated INF-γ ( OR: 3. 710, 95 % CI:1. 584-5. 836) were independent risk factors for the occurrence of ATB (P< 0. 05). Conclusion IP-10, IL-2, MCP-1, and INF-γ are highly expressed in ATB, and elevated levels of IP-10, IL-2, MCP-1, and INF-γ are risk factors for the occurrence of ATB. The combined use of IP-10, IL-2, MCP-1, and INF-γ in the diagnosis of ATB can improve the accuracy of the results. Related Articles | Metrics Select Effect of miR-377-3p on Proliferation and Apoptosis of Epithelial Ovarian Cancer SKOV3 Cells #br# SHEN Mengxing, YAO Hairong, WANG Zhenying Journal of Medical Molecular Biology    2025, 22 (5): 482-487.   DOI: 10.3870/j.issn.1672-8009.2025.05.010 Abstract （91）      PDF （3566KB）（18）       Knowledge map    Save Objective To explore the effect of microRNA-377-3p ( miR-377-3p) on the proliferation and mitochondrial function of epithelial ovarian cancer (EOC) SKOV3 cells by targetingE-box binding zinc finger protein 2 (ZEB2). Methods SKOV3 cells were cultured in vitro, cellswith miR-377-3p and ZEB2 overexpression were constructed, and the proliferation, apoptosis, mitochondrial membrane potential, and oxidative stress in cells were detected. Results The expression level of ZEB2 was inhibited by miR-377-3p. Compared with those in the control group, the number of colony formation was decrease, the expression levels of Ki67, PCNA, Survivin, and the level of SOD were decreased in the miR-377-3p group, while the apoptosis rate, the proportion of JC-1 green fluorescence, the level of MDA, and the ratios of Bax / Bcl-2, cleaved caspase-3 /caspase-3 and cleaved caspase-9 / caspase-9 were increased (P < 0. 05). In addition, the number ofcolony formation, the expression levels of Ki67, PCNA, Survivin, and the level of SOD were increased in the ZEB2 group, while the apoptosis rate, proportion of JC-1 green fluorescence, the level of MDA, and the ratios of Bax / Bcl-2, cleaved caspase3 / caspase3 and cleaved caspase9 /caspase9 were decreased ( P < 0. 05 ). The overexpression of ZEB2 in the miR-377-3p + ZEB2 groups could partially reverse the effect of miR-377-3p (P < 0. 05). Conclusion miR-377-3p caninhibit the ZEB2 expression, reduce the membrane potential, enhance the oxidative stress, inhibit the proliferation, and promote the apoptosis of ovarian cancer SKOV3 cells. Related Articles | Metrics Select Effect of Adiponectin on Endometrial Cancer Cell Growth, Invasion, and PI3K / AKT / NF-κB Pathway #br# QIAO Meiling, ZHANG Lihua Journal of Medical Molecular Biology    2025, 22 (5): 488-493.   DOI: 10.3870/j.issn.1672-8009.2025.05.011 Abstract （80）      PDF （4541KB）（10）       Knowledge map    Save Objective To explore the effect of adiponectin on the proliferation, invasion, andphosphatidylinositol 3-kinase / protein kinase B / nuclear factor kappa B (PI3K / AKT / NF-κB) pathway in endometrial cancer cells. Methods Endometrial cancer cell lines AN3CA and HEC-1-Awere transfected with pcDNA, pcDNA-adiponectin. The efficiency of adiponectin overexpression were detected by RT-PCR and Western blotting. Cell proliferation, cell apoptosis, and cell invasion were detected by CCK8, flow cytometry, and Transwell assay, respectively. The expression levels of caspase-9, caspase-3, vascular endothelial growth factor ( VEGF), E-cadherin, N-cadherin, fibronectin ( FN ), p-PI3K / PI3K, p-AKT / AKT, p-P65 / P65 were detected by Western blotting. Results Compared with those in the Control group, the adiponectin expression levels of endometrial cancer cells AN3CA and HEC-1-A in the adiponectin group were significantly increased(P < 0. 05), the cell proliferation ratio was significantly reduced (P < 0. 05), and the rate of apoptosis was significant increase (P < 0. 05), cell invasion number was significantly reduced (P <0. 05), the expression levels of caspase-9 and caspase-3 were significantly increased (P < 0. 05),VEGF levels were significantly decreased (P< 0. 05), E-cadherin level was increased, N-cadherinand FN levels were decreased (P< 0. 05), phosphorylated PI3K / AKT / P65 levels were significantly decreased (P< 0. 05). Conclusion Adiponectin inhibits the proliferation and invasion of endometrial cancer AN3CA and HEC-1-A cells and the activation of PI3K / AKT / NF-κB pathway. Related Articles | Metrics Select Effect of STAT3 on Proliferation and Autophagy of Colorectal Cancer Stem Cells by Wnt / β-catenin Signaling Pathway #br# WANG Linlin, Yan Weijiao Journal of Medical Molecular Biology    2025, 22 (5): 494-499.   DOI: 10.3870/j.issn.1672-8009.2025.05.012 Abstract （86）      PDF （2092KB）（17）       Knowledge map    Save Objective To investigate the effect of signal transducer and activator of transcription 3 (STAT3) on the proliferation and autophagy of colorectal cancer stem cells. Methods The colorectal cancer stem cells were sorted out from colorectal cancer cells, and were categorized into 4groups: CCSC, STAT3, STAT3 ihibitor, and STAT3 inhibitor + Wnt / β-catenin-inhibitor. The proliferation rate, apoptosis rate, and the expression levels of proteins related to cell proliferation, apoptosis, and autophagy, as well as Wnt / β-catenin signaling pathway proteins, were measured ineach group. Results The expression levels of STAT3 in cancer tissues and CD133 + CD44 + cellswere significantly higher than those in the adjacent tissues and CD133 - CD44 - cells ( P < 0. 05). Compared to the CCSC group, the STAT3 group showed increased expression levels of STAT3, CyclinD1, Bcl-2, P62, Wnt2, and β-catenin, as well as higher proliferation rates, while the apoptosis rate and the expression levels of Caspase-3, Bax, and Beclin1 were reduced. Compared to both the CCSC and STAT3 groups, the STAT3 ihibitor group and the STAT3 inhibitor + Wnt / β- catenin-inhibitor group showed decreased expression levels of STAT3, CyclinD1, Bcl-2, P62, Wnt2, and β-catenin, as well as lower proliferation rates, while the apoptosis rate and the expression of Caspase-3, Bax, and Beclin1 were increased (P < 0. 05). Compared to the STAT3 ihibitorgroup, the STAT3 inhibitor + Wnt / β-catenin-inhibitor group showed decreased expression levels of STAT3, CyclinD1, Bcl-2, P62, Wnt2, and β-catenin, as well as lower proliferation rates, while the apoptosis rate and the expression levels of Caspase-3, Bax, and Beclin1 were increased(P< 0. 05). Conclusion Downregulation of STAT3 inhibits the proliferation, and enhances the apoptosis and autophagy of colorectal cancer stem cells. The mechanism may be related to the inhibition of the Wnt / β-catenin signaling pathway. Related Articles | Metrics Select Research Progress of Fruquintinib in Colorectal Cancer #br# XIE Yejie, QIN Ziheng, YANG Chaogang, Journal of Medical Molecular Biology    2025, 22 (5): 500-507.   DOI: 10.3870/j.issn.1672-8009.2025.05.013 Abstract （96）      PDF （880KB）（48）       Knowledge map    Save Fruquintinib is a novel and highly selective inhibitor of vascular endothelial growthfactor receptor (VEGFR), which plays an important role in the comprehensive treatment of colorectal cancer (CRC). Numerous studies have shown that fruquintinib can effectively block tumor angiogenesis and has demonstrated significant efficacy and good tolerance in the treatment of metastatic CRC. This review aims to summarize and discuss the pharmacological mechanism, pharmacokinetic characteristics, adverse event of fruquintinib, as well as the results of a series of clinical trials in CRC. Additionally, this review explores the potential of combining VEGFR inhibitors with other therapies, providing new directions for further optimizing its use in personalized treatment. Related Articles | Metrics Select Mechanism and Application Prospects of LINE-1 Transposons in Cellular Senescence and Age-Related Diseases #br# WANG Chenhui, LIU Pengpeng, ZHANG Rui Journal of Medical Molecular Biology    2025, 22 (5): 508-515.   DOI: 10.3870/j.issn.1672-8009.2025.05.014 Abstract （99）      PDF （2116KB）（41）       Knowledge map    Save The long interspersed nuclear element-1 ( LINE-1) is the only retrotransposon inthe human genome capable of autonomous activity, and it plays an essential role in regulating many physiological processes. Its activity is closely connected to cellular aging and the overall aging of theorganism. Normally, LINE-1 remains tightly suppressed through epigenetic mechanisms such asDNA methylation. However, during aging or cellular stress, this control can become disrupted,leading to abnormal activation of LINE-1. When activated inappropriately, LINE-1 can cause harmthrough several pathways, including creating DNA double-strand breaks, inserting itself into new locations in the genome ( insertional mutagenesis), and triggering the cGAS-STING immune response pathway. These effects contribute to genomic instability and promote the formation of the senescence-associated secretory phenotype ( SASP). Collectively, these processes worsen telomere dysfunction and increase the risk of age-related diseases like cancer, neurodegenerative conditions,and heart disease. This review emphasizes how dysregulated LINE-1 activity considerably contributesto aging and related diseases. It focuses on its main mechanisms, particularly how it accelerates disease progression by destabilizing the genome and altering epigenetic regulation. What ’ s more,LINE-1 shows promise as a biomarker for age-associated conditions and as a potential target for therapeutic intervention. Related Articles | Metrics Select Data Visualization Analysis of Biochemistry AI Textbooks Applied to Large-scale Personalized Teaching #br# YANG Ziyan, ZHANG Xiang, YUAN Yuqiang, ZHAO Jing Journal of Medical Molecular Biology    2025, 22 (5): 516-523.   DOI: 10.3870/j.issn.1672-8009.2025.05.015 Abstract （78）      PDF （10636KB）（17）       Knowledge map    Save While artificial intelligence ( AI) textbooks offer the advantage of enabling largescale personalized teaching, they face the new challenge of difficulty in visualizing massive learning data. This study systematically analyzed the learning behaviors of 436 students using the AI textbookMedical Biochemistry, addressing three critical challenges in data visualization: ① visualizing interclass variations across parallel large classes; ② analyzing the fine-grained subgroup learning profiles within a parallel large class; ③ profiling the in-depth thinking reflected in AI interactions within a parallel large class. In this research, seven key parameters were used to demonstrate the differences in learning characteristics between parallel large classes. Within one parallel large class, students were subdivided into 9 subgroups based on behavioral heterogeneity, with personalized differences analyzed across subgroups. Using a self-developed scaffold questioning framework for AI interactions, cluster analysis was conducted on all interaction questions between students and AI in one parallel large class, enabling visual evaluation of students’in-depth thinking effects. Future research should develop an automatic display for AI textbook data visualization based on these strategies to support data-driven decision-making in large-scale personalized teaching. Related Articles | Metrics Select Practice and Exploration on Profound Integration of Ideological and Political Education in Biochemistry and Molecular Biology Curriculum Based on BOPPPS Model and Perspective of “Comprehensive Ideological and Political Education” #br# HE Wenhui, CHEN Shan, ZHONG Dan, WANG JingΔ, DAI ShuangshuangΔ Journal of Medical Molecular Biology    2025, 22 (5): 524-530.   DOI: 10.3870/j.issn.1672-8009.2025.05.016 Abstract （94）      PDF （4579KB）（204）       Knowledge map    Save From the perspective of the “Comprehensive Ideological and Political Course”, it is a key strategic measure to fully display the educational effectiveness of the Biochemistry and Molecular Biology course in medical colleges and promote the integration and innovation of the “ Comprehensive Social Classroom” and the “Ideological and Political Education in Small Classrooms” to achieve the achieve the fundamental task of forstering virtue through education. Based on the characteristics of the teaching content of Biochemistry and Molecular Biology and the “BOPPPS” teachingmodel, this study takes internal drive, humanistic charm, scientific view, world eye, and Chinese heart as the top-level design of ideological and political education in the course. In addition, it adopts the dual strategies of “bringing in and going out”, making full use of social resources such as museums and red culture bases, besides innovating the ideological and political education classroom in the course with the teaching method of knowledge and ideology spiraling upward. In conclusion, the research results show that this innovative model significantly improves the effectiveness of ideological and political education in the course, enhances students’ideological realm and comprehensive quality, and provides new ideas and practical examples for the implementation of curriculum ideological and political education in the whole domain of biochemistry and molecular biology course under the perspective of “Comprehensive Ideological and Political Education” . Related Articles | Metrics Select Role of ClC-7 in Biogenesis of Lamellar Body in Alveolar Type Ⅱ Cells ZHOU Zixuan, HAO Zhenhua, LI Wei Journal of Medical Molecular Biology    2025, 22 (6): 531-538.   DOI: 10.3870/j.issn.1672-8009.2025.06.001 Abstract （75）      PDF （9374KB）（29）       Knowledge map    Save Objective To explore the role of ClC-7 in lamellar body(LB)biogenesis and to investigate the possible pathogenesis of some ClC-7 mutants from patients. Methods siRNA knockdown was employed to decrease the expression of ClC-7 in A549 cells,followed by observing LB morphological changes using laser confocal microscopy and transmission electron microscopy.Wild-type and mutant ClC-7 plasmids were constructed,and the co-localization of ClC-7 with LB and other organelles was observed using immunofluorescence method. Results ClC-7 was localized to LBs and lysosomes.The size of LBs in the ClC-7 knockdown cells was enlarged.Mutations of p.G203D,p.G215R,p.G292E,p.R403Q,and p.L766P,led to mislocalization of ClC-7 to the endoplasmic reticulum.Mutation of p.P470L lead to partial retention of ClC-7 on early endosomes but mostly localizes on LBs. Conclusion ClC-7 in A549 cells is localized to both LBs and lysosomes.Knockdown of ClC-7 in cultured cells leads to enlarged LBs.Most of the mutated ClC-7 cannot be correctly localized on lamellar bodies and lysosomes. Reference | Related Articles | Metrics Select LncRNA GAS5 Regulates Th17/Treg Imbalance in Celiac Disease by Targeting miR-155 FENG Yan, LI Ting, WANG Man, LIU Weidong, WANG Chun, GAO Feng Journal of Medical Molecular Biology    2025, 22 (6): 539-547.   DOI: 10.3870/j.issn.1672-8009.2025.06.002 Abstract （58）      PDF （11672KB）（12）       Knowledge map    Save Objective To investigate how long non-coding RNA(lncRNA)GAS5 regulates Th17/Treg imbalance through targeting miR-155 in celiac disease(CeD). Methods Peripheral blood was collected from 20 CeD patients(CeD group)and 20 healthy individuals without CeD or other autoimmune diseases(healthy group),CD4+T cells were isolated from both groups.the expression levels of lncRNA GAS5 and miR-155 in CD4+T cells from CeD patients and the control group were dected by qRT-PCR.Flow cytometry was used to analyze the Th17/Treg ratio.Pearson statistical analysis was performed to evaluate the correlation between the expression levels of lncRNA GAS5 and miR-155 with the Th17/Treg ratio in CeD patients.In vitro,CD4+T cells from the CeD patients were divided into 7 groups:control group,pcDNA3.1-NC group,pcDNA3.1-GAS5 group,miR-NC group,miR-155-mimics group,pcDNA3.1-GAS5+miR-NC group,and pcDNA3.1-GAS5+miR-155-mimics group.qRT-PCR was used to detect the expression levels of lncRNA GAS5 and miR-155 in each group.Edu staining and Hoest33342 staining was used to detect the proliferation and apoptosis of CD4+T cells,respectively.Immunofluorescence staining was used to measure the expression of IL-17 and Foxp3.Flow cytometry was used to detect the proportion of IL-17+ and Foxp3+ cells in each group. Results Compared to those in the healthy group,the expression level of lncRNA GAS5 in the CeD group was decreased,while the expression level of miR-155 was increased.lncRNA GAS5 was negatively correlated with the Th17/Treg ratio(r=-0.65,P<0.05),and miR-155 was positively correlated with the Th17/Treg ratio(r=0.70,P<0.05).In CD4+T cells from the CeD group,the pcDNA3.1-GAS5 group showed increased expression levels of lncRNA GAS5 and Foxp3,increased proliferation rate of CD4+T cells,and increased proportion of Foxp3+ cells(allP<0.05),while the expression levels of miR-155 and IL-17,the apoptosis rate of CD4+T cells,and the proportion of IL-17+ cells were decreased(allP<0.05)when compared with those in the pcDNA3.1-NC group.When compared with the miR-NC group,the miR-155-mimics group showed decreased Foxp3 expression level,decreased proliferation rate of CD4+T cells,and decreased proportion of Foxp3+ cells(allP<0.05),while the expression levels of miR-155 and IL-17,the apoptosis rate of CD4+T cells,and the proportion of IL-17+ cells were increased(allP<0.05).Compared with the pcDNA3.1-GAS5+miR-NC group,the pcDNA3.1-GAS5 + miR-155-mimics group showed decreased Foxp3 expression level,decreased proliferation rate of CD4+T cells,and decreased proportion of Foxp3+ cells(allP<0.05),while the expression levels of miR-155 and IL-17,the apoptosis rate of CD4+T cells,and the proportion of IL-17+ cells were increased(allP<0.05). Conclusion lncRNA GAS5 regulates Th17/Treg imbalance by targeting miR-155,affecting the proliferation and apoptosis of CD4+T cells in CeD patients,thereby influencing IL-17 and Foxp3 expression.This suggests that lncRNA GAS5 may serve as a potential therapeutic target for CeD. Reference | Related Articles | Metrics Select Wnt 5a/Smad 2/3 Activation and Sclerostin Inhibition in Subchondral Bone Cells Promote Trabecular Sclerosis in Osteoarthritis Ekermujiang Arken, HAN Xiaoping, CUI Yong, HUANG Tao Journal of Medical Molecular Biology    2025, 22 (6): 548-556.   DOI: 10.3870/j.issn.1672-8009.2025.06.003 Abstract （62）      PDF （6169KB）（9）       Knowledge map    Save Objective To investigate the effect of Wnt 5a/Smad 2/3 activation and sclerostin inhibition in subchondral bone cells on trabecular sclerosis in osteoarthritis. Methods The co-cultured system of chondrocytes and osteoblasts was established.Cells were divided into 5 groups:Control group,OE-vector group,LIF OE group,shRNA-NC group and shRNA-LIF group.RNA immunoprecipitation(RIP)was used to detect the direct interaction between LIFR and sclerostin encoding gene SOST mRNA.The relative expression levels of SOST mRNA was detected by qRT-PCR.LIF expression in chondrocytes was overexpressed or knocked-down,and the relative expression levels of LIF and LIFR was detected by Western blotting.fourty male C57BL 6J mice aged 7-8 weeks were randomly divided into 7 groups:Control group,Model group,Sham group with 4-week or 8-week induction,and Model+LIFR antagonist group with 8-week induction.Micro-CT was used to measure the bone volume fraction(BV/TV),trabecular thickness(Tb.Th)and trabecular number(Tb.N).HE staining and safranin O-fast green staining were used to analyze the histopathological changes in mice joint tissues.The relative expression levels of Wnt 5a,Smad 2/3,Sclerostin,leukemia inhibitory factor(LIF)/LIF receptor(LIFR),tartrate-resistant acid phosphatase(TRAP)and matrix metalloproteinases 13(MMP-13)were detected by Western blotting. Results RIP results showed that LIFR and SOST mRNA had direct interaction.Overexpression of LIF increased LIFR expression levels(P<0.05)and decreased Sclerostin expression levels(P<0.05);knocking down LIF produced the opposite results.After 8 weeks of induction,the BV/TV and Tb.Th were increased(P<0.05),and the Tb.N was decreased(P>0.05)in the Model group when compared with those in the Sham group.Compared with those in the Model group,the BV/TV and Tb.Th were decreased(P<0.05)in the Model+LIFR antagonist group,and the Tb.N was increased(P>0.05).HE staining and Safranin O-fast green cartilage staining results showed that in the Model group,cartilages was destroyed,the intercellular matrix degraded,cell arrangement was disrupted,the cartilage layer disintegrated,and the subchondral bone was affected.In the Model+LIFR antagonist group,the cartilage surfaces area and proliferation area were destroyed,but the hypertrophy zone remained relatively intact,suggesting that cartilage zone destruction was relatively alleviated following LIFR antagonist treatment.After 4 weeks or 8 weeks of induction,the expression levels of Wnt 5a,p-Smad 2/3 in the Model group were increased(P<0.05),the expression levels of sclerostin was decreased(P<0.05),and the expression levels of LIF,LIFR,TRAP and MMP-13 were up-regulated(P<0.05)when compared with those in the Sham group. Conclusion Wnt 5a/Smad 2/3 activation and sclerostin inhibition in subchondral bone cells promote trabecular sclerosis. Reference | Related Articles | Metrics Select Effect of miR-214-5p on DNA Damage and Chemotherapy Sensitivity in Neuroblastoma Cells by Regulation of FANCA ZHAO Conghui, LIU Bing, LIU Jiajia, CUI Ling, LIU Xiaoxia, LEI Jianhua Journal of Medical Molecular Biology    2025, 22 (6): 557-562.   DOI: 10.3870/j.issn.1672-8009.2025.06.004 Abstract （57）      PDF （5204KB）（7）       Knowledge map    Save Objective To explore the effect and mechanism of microRNA-214-5p(miR-214-5p)on DNA damage and chemotherapy sensitivity in neuroblastoma(NB). Methods The relationship between Fanconi anemia complementary group A (FACNA) protein and clinicopathological characteristics of NB was analyzed by TARGET database.NB cell lines with low expression of miR-214-5p and overexpression/low expression of FANCA were constructed,and their effects on the proliferation of NB in vivo and in vitro were detected by cell counting kit-8(CCK-8)and transplanted tumor model.The targeted relationship between miR-214-5p and FANCA was verified. Results FANCA was screened out as the intersection gene correlated with NB in GEO and TARGET databases,and its expression level was related to cells proliferation pathways,and the prognosis and clinicopathological characteristics of NB.Compared with those in the empty vector(Vector)group,the cells viability,and the volume and weight of transplanted tumors were increased in the FANCA group(P<0.05).Compared with those in the shNC group,the cells viability was decreased in the shFANCA1/2 groups(P<0.05).Compared with those in the control group,the phosphorylated histone γ-H2AX was increased after treated with 1 mmol/L H2O2(P<0.05),but γ-H2AX was decreased after FANCA overexpression(P<0.05).With the increase of doxorubicin concentration,cells viability was decreased,but it was higher in the FANCA group than in the Vector group(P<0.05).There was a targeted relationship between miR-214-5p and FANCA. Conclusion miR-214-5p can inhibit the proliferation of NB cells by reducing FANCA expression level,and regulate the DNA damage and chemotherapy sensitivity in cells. Reference | Related Articles | Metrics Select Effect of Sodium Butyrate on Infiltrated Treg and Th17 Proportion in Adipose Tissues and Insulin Sensitivity in Type 2 Diabetic Mice WANG Siyao, GAO Jing, ZHANG Chunxue, LUO Li, JIN Jin Journal of Medical Molecular Biology    2025, 22 (6): 563-570.   DOI: 10.3870/j.issn.1672-8009.2025.06.005 Abstract （57）      PDF （5492KB）（4）       Knowledge map    Save Objective To explore the immunological mechanisms of sodium butyrate on improving Type 2 diabetic mouse model’s insulin sensitivity. Methods Type 2 diabetic mouse model was established by feeding with a high-fat/high-sucrose diet combined with streptozotocin induction.Thirty male C57BL/6 mice were divided into three groups:control group,model group,model+sodium butyrate group,10 mice in each group.The values of glucose tolerance test and insulin tolerance test were measured.The proportion of infiltrated regulatory T cells(Treg)(%)and T helper type 17(Th17)(%)in mice peripheral blood and adipose tissues were measured by flow cytometry.Western blotting was used to determine the relative expression levels of p-mTOR,mTOR,p-p70S6K and p70S6K in infiltrated Treg and Th17 cells in adipose tissues. Results Glucose tolerance test results have shown that compared with control group,in model+sodium butyrate group blood glucose levels increased at 20 min(P<0.05);there was no statistically significant difference in blood glucose at subsequent time points(P>0.05).Insulin tolerance test results have shown that there was no significant difference in blood glucose levels in model+sodium butyrate group at any time points(P>0.05).Compared with those in the control group,the percentage(%)of infiltrating Th17 cells in peripheral blood and adipose tissues was increased in the model group(P<0.05),and the percentage(%)of infiltrating Treg cells was decreased(P<0.05),and the relative expression levels of p-mTOR and p-p70S6K in infiltrated Treg cells and Th17 cells in adipose tissues were increased(P<0.05).Compared with the model group,the model+sodium butyrate group significantly reversed the above indicator values(P<0.05). Conclusion Sodium butyrate treatment could inhibit the activation levels of mTOR/p70S6K signaling pathway,regulate the numbers of Treg cells and Th17 cells in peripheral blood and adipose tissues,and improve insulin sensitivity in type 2 diabetes mice model. Reference | Related Articles | Metrics Select Oxysophocarpine Induces Apoptosis of Breast Cancer Cells by Inhibition of Nrf2/HO-1 Signaling Pathway CUI Min, ZHANG Tong, SI Mengyuan, LIN Ying, XIE Wenjie, SUN Jirui Journal of Medical Molecular Biology    2025, 22 (6): 571-578.   DOI: 10.3870/j.issn.1672-8009.2025.06.006 Abstract （50）      PDF （6035KB）（4）       Knowledge map    Save Objective To investigate the effect of oxysophocarpine on breast cancer(BC)cell proliferation,apoptosis,and oxidative stress by modulating the nuclear factor erythroid 2-related factor 2,(Nrf2)/ heme oxygenase-1(HO-1)/ NAD(P)H:quinone oxidoreductase 1(NQO1)pathway. Methods MDA-MB-231 and MCF-7 cell lines were used.Cell viability was detected by CCK-8 assay.Quantitative real-time polymerase chain reaction(qRT-PCR)or Western blotting were used to measure the expression level of proliferation-related(Survivin,Ki67,P21),apoptosis-related(cleaved caspase-3/9,Bax/Bcl-2 ratio),and Nrf2/HO-1/NQO1 pathway-related moleculars.Apoptosis and mitochondrial membrane potential were analyzed by flow cytometry.Oxidative stress markers superoxide dismutase(SOD),glutathione(GSH),malondialdehyde(MDA))were assessed via enzyme-linked immunosorbent assay(ELISA).Nrf2 was overexpressed in MDA-MB-231 cells to validate the Nrf2/HO-1/NQO1 pathway’s effect.A nude mouse xenograft model was established to evaluate tumor growth,Ki67 expression,caspase-3 positivity,apoptosis rate(TUNEL),and Nrf2/HO-1/NQO1 pathway protein expression levels. Results Oxysophocarpine inhibited BC cell viability,induced apoptosis,and reduced mitochondrial membrane potential in a dose-dependent manner.It significantly suppressed the expression of proliferation-related molecules(Survivin,Ki67),and promoted the expression of apoptosis-related molecules(P21,cleaved caspase-3/9,Bax/Bcl-2 ratio).Additionally,it inhibited Nrf2/HO-1/NQO1 pathway activation and exacerbated oxidative stress(reduced SOD,GSH;increased MDA).Nrf2 overexpression partially reversed these effects of oxysophocarpine.Animal experiments confirmed that oxysophocarpine inhibited tumor growth,reduced proliferation(Ki67),promoted apoptosis(caspase-3,TUNEL),and suppressed Nrf2 pathway activation in vivo. Conclusion Oxysophocarpine effectively inhibits breast cancer cell proliferation,induces apoptosis,and enhances oxidative stress by suppressing the Nrf2/HO-1/NQO1 signaling pathway. Reference | Related Articles | Metrics Select Effect of circRNA VAPA/miR-377-3p/ZEB2 Axis on Paclitaxel Resistance of Breast Cancer SONG Yunjie, LIANG Jia, XU Bin, ZHANG Penghui, WEI Limin Journal of Medical Molecular Biology    2025, 22 (6): 579-585.   DOI: 10.3870/j.issn.1672-8009.2025.06.007 Abstract （57）      PDF （1574KB）（3）       Knowledge map    Save Objective To investigate the role of circular RNA vesicle-associated membrane protein-associated protein A(circRNA VAPA)on Zinc-finger E-box binding homeobox 2(ZEB2)in paclitaxel resistance of breast cancer by targeting miR-377-3p. Methods Human breast cancer cell line MCF7 and paclitaxel-resistant strain MCF7/Taxol were cultured,and the expression level of circVAPA,miR-377-3p and ZEB2 were detected and compared.MCF7/Taxol cells were divided into 9 groups.Dual luciferase reporter gene assay was used to detect the targeting relationship between circVAPA and miR-377-3p,and that between miR-377-3p and ZEB2.Cell proliferation inhibition rate was measured by CCK-8 assay and the sensitivity to paclitaxel was assessed. Results The expression levels of circVAPA and ZEB2 in the MCF7/Taxol cells were higher than those in the MCF7 cells,and the expression levels of miR-377-3p were lower than those in the MCF7 cells(P<0.05).The activities of circVAPA and ZEB2 wild-type reporter genes in the miR-377-3p mimic group were both lower than those in the NC group(P<0.05),while there was no significant difference in the activities of circVAPA and ZEB2 mutant reporter genes(P>0.05).Compared with those in the NC group,the paclitaxel sensitivity of the si-circVAPA group and the miR-377-3p mimic group were increased(P<0.05),and the expression level of ZEB2 were decreased(P<0.05).Compared with those in the control plasmid group,the paclitaxel sensitivity in the circVAPA group was decreased,and the expression level of ZEB2 was increased.Compared with those in the circVAPA group,the paclitaxel sensitivity in the circVAPA+miR-377-3p group was increased,and the expression level of ZEB2 was decreased(P<0.05).The paclitaxel sensitivity of MCF7/Taxol cells in the si-circVAPA+miR-377-3p inhibitor group was lower than that in the si-circVAPA group(P<0.05),and the expression level of ZEB2 was higher than that in the si-circVAPA group(P<0.05). Conclusion The regulation of ZEB2 by circular RNA VAPA/miR-377-3p is related to paclitaxel resistance in breast cancer cells. Reference | Related Articles | Metrics Select Identification and Immunological Characteristics of Migrasome-related Genes in Prostate Cancer CHEN Shasha, CAI Weiwang, LUO Jiamei, ZHANG Yong Journal of Medical Molecular Biology    2025, 22 (6): 586-593.   DOI: 10.3870/j.issn.1672-8009.2025.06.008 Abstract （46）      PDF （9776KB）（7）       Knowledge map    Save Objective To explore the expression patterns of migrasome-related genes(MRGs)in prostate cancer and elucidate their underlying mechanisms using bioinformatics tools. Methods Transcriptomic data of 498 cases of prostate cancer were obtained from The Cancer Genome Atlas(TCGA)database.The limma package was used to identify differentially expressed genes in prostate cancer tissues,and the results were validated using GSE70770 and GSE88808 datasets.Migrasome-related differentially expressed genes(MRDEGs)were screened using protein annotation databases.Gene Ontology(GO)was applied to investigate the functional enrichment of MRDEGs.The LASSO regression and SVM-RFE model were used to screen key diagnostic MRDEGs for prostate cancer,and a predictive Nomogram was constructed.The correlation between 22 types of infiltrating immune cells and MRDEGs was analyzed. Results Six MRDEGs were identified in prostate cancer tissues.PKD1,ITGB1 and ITGA5 were significantly expressed in the GSE70770 and GSE88808 datasets.GO enrichment analysis showed that these genes were primarily enriched in biological processes or molecular functions such as the positive regulation of cyclin-dependent serine/threonine protein kinase activity,calcium channel activity,and transmembrane transporter binding.Machine learning identified ITGB1 and ITGA5 as the key MRDEGs for diagnosing prostate cancer.The prediction model constructed based on the key MRDEGs for prostate cancer in the training set TCGA database had an AUC value of 0.833,and the AUC value in the external validation set GSE70770 was 0.868.Resting dendritic cells and neutrophils showed a positive correlation with the expression levels of ITGB1 and ITGA5,while regulatory T cells(Tregs)and M0 macrophages showed a negative correlation. Conclusion Our study employed bioinformatics methods to systematically elucidate the significant role of the migration-related genes ITGB1 and ITGA5 in the pathogenesis of prostate cancer,potentially providing new insights into molecular targets for the treatment of prostate cancer. Reference | Related Articles | Metrics Select Renal Cancer Cell Exosomes Inhibit Tumor Killing Function of CD8+T Cells by Upregulation of PD-1 WANG Lei, LI Qian, LIU Xin, LIU Guolu, WANG Yijin, ZHANG Chengbo Journal of Medical Molecular Biology    2025, 22 (6): 594-600.   DOI: 10.3870/j.issn.1672-8009.2025.06.009 Abstract （53）      PDF （2214KB）（3）       Knowledge map    Save Objective To investigate the effect of renal cancer cell exosome on CD8+T cell tumor killing fuction. Methods HK-2 exo,786-O exo,SN12-PM6 exo,and an equal volume of PBS were co-cultured with CD8+T cells,cytotoxicity assay was used to detect the killing function of CD8+T cells.ELISA was used to detect the secretion of IFN-γ,IL-2 and TNF-α.Western blotting was used to detect the expression level of PD-1 in CD8+T cells.CD8+T cell transfected PD-1 siRNA(si-PD-1)and siRNA Negative Control(si-NC)were co-incubated with 786-O exo and SN12-PM6 exo for 24 hours,respectively.Cytotoxicity experiments were conducted to detect the cytotoxicity of CD8+T cells against 786-O and SN12-PM6 cells after transfection. Results Compared with those in the PBS group,the secretion of IFN-γ,IL-2 and TNF-α in the 786-O exo group and SN12-PM6 exo group were significantly downregulated(P<0.05).The ability to kill 786-O and SN12-PM6 was significantly reduced(P<0.05),and PD-1 protein expression level was significantly upregulated(P<0.05).After co-incubation with 786-O exo and SN12-PM6 exo,the the secretion of IFN-γ,IL-2 and TNF-α,as well as the ability to kill 786-O and SN12-PM6 were significantly increased when compared with those in the CD8+T cells transfected with si-NC(P<0.05). Conclusion Renal cancer exosome can induce the expression of PD-1 of CD8+T cells to inhibit the tumor killing function. Reference | Related Articles | Metrics Select LncRNA MIR100HG Promotes Epithelial-mesenchymal Transition in Triple-negative Breast Cancer MDA-MB-231 Cells LI Changchun, YAN Wenyue, LIU Genxiang, ZHOU Guangjun Journal of Medical Molecular Biology    2025, 22 (6): 601-606.   DOI: 10.3870/j.issn.1672-8009.2025.06.010 Abstract （52）      PDF （4907KB）（3）       Knowledge map    Save Objective To investigate the effect of long non-coding RNA(lncRNA)MIR100HG on epithelial-mesenchymal transition(EMT)of triple-negative breast cancer MDA-MB-231 cells. Methods MIR100HG was overexpressed or inhibited in the MDA-MB-231 cells,cell proliferation was measured by MTS assay,cell apoptosis rate was analyzed by flow cytometry,and cell migration and invasion were determined by Transwell assay.Western blotting was used to detect the regulatory effect of MIR100HG on epithelial-mesenchymal transition related markers. Results Overexpression of MIR100HG promoted the proliferation,migration and invasion of MDA-MB-231 cells,reduced cell apoptosis,downregulated the expression of epithelial markers and upregulated the expression of mesenchymal markers; Inhibition of MIR100HG produced opposite results. Conclusion Overexpression of LncRNA MIR100HG can promote the proliferation,migration and invasion of MDA-MB-231 cells,reduce the apoptosis of MDA-MB-231 cells,and induce the epithelial-mesenchymal transition of MDA-MB-231 cells. Reference | Related Articles | Metrics Select Correlation of Serum Defensin 5 Level and Severe Acute Pancreatitis Complicated with Peripancreatic Necrosis ZHANG Hongyan, CHEN Hui Journal of Medical Molecular Biology    2025, 22 (6): 607-611.   DOI: 10.3870/j.issn.1672-8009.2025.06.011 Abstract （48）      PDF （1210KB）（2）       Knowledge map    Save Objective To study the correlation of serum defensin 5 level and severe acute pancreatitis(SAP)complicated with peripancreatic necrosis. Methods A retrospective study was conducted on 224 SAP patients admitted to Kunshan Hospital of Traditional Chinese Medicine from May 2020 to December 2023,and they were divided into peripancreatic necrosis group(n=96)and non-peripancreatic necrosis group(n=128)according to whether peripancreatic necrosis infection occurred.Compare the differences in general characteristics,and serum defensin 5 levels and laboratory indicators within 24 hours of admission between the two groups.Logistic regression was used to analyze the influencing factors of SAP combined with peripancreatic necrosis,and receiver operating characteristics(ROC)curve was used to analyze the diagnostic indicators of peripancreatic necrosisn. Results The levels of serum defensin 5 and serum calcium in the peripancreatic necrosis group were lower than those in the non-peripancreatic necrosis group,and the time from onset to hospital admission,the levels of C-reactive protein(CRP)and procalcitonin(PCT)were higher than those in the non-peripancreatic necrosis group(P<0.05).Logistic regression analysis showed that the level of serum defencin 5,the time from onset to admission,and the levles of serum calcium,CRP and PCT were the influencing factors of peripancreatic necrosis(P<0.05).ROC curve analysis demonstrated that serum defensin 5 level,time from symptom onset to admission,serum calcium levels,CRP,and PCT levels—both individually and in combination—possess diagnostic value for SAP complicated by peripancreatic necrosis infection.The combined diagnostic approach achieved a sensitivity of 82.81 % and a specificity of 96.99 %. Conclusion The decrease of serum defensin 5 level is related to SAP complicated with peripancreatic necrosis.The combination of defensin 5 and time from onset to hospital admission,serum calcium,CRP and PCT have better diagnostic efficacy for SAP complicated with peripancreatic necrosis. Reference | Related Articles | Metrics Select Problems in Detecting HER2 in Breast Cancer by Using Immunohistochemistry and Fluorescence in Situ Hybridization ZHANG Xinjuan, WEI Xiaoyun, LI Xiaofeng, LIU Xi, OU Da, KANG Yan, ZHAO Xiao-ni, YANG Zhe, WANG Yuanyuan Journal of Medical Molecular Biology    2025, 22 (6): 612-616.   DOI: 10.3870/j.issn.1672-8009.2025.06.012 Abstract （49）      PDF （1568KB）（2）       Knowledge map    Save Objective To explore the problems of immunohistochemistry and fluorescence in situ hybridization in HER2 detection of breast cancer. Methods A total of 309 HER2 IHC 2+ breast cancer samples underwent FISH analysis,including 159 specimens submitted at our hospital in 2018,54 specimens between 2010 and 2012,and 96 specimens from external hospitals between 2016 and 2019. Results The positive rate of FISH test results for breast cancer HER2 IHC 2+ cases in 2018 was significantly lower than that of specimens from other hospitals and the hospital from 2010 to 2012. Conclusion Patients with breast cancer expected to undergo HER2-targeted therapy,particularly those from subordinate hospitals or diagnosed at an early stage,should be further tested using immunohistochemical analysis or FISH to guide precision medicine. Reference | Related Articles | Metrics Select Advances in Researches on RIG-I in Diseases WANG Wenliang, TIAN Haiping, LIU Taiyi, WANG Cheng Journal of Medical Molecular Biology    2025, 22 (6): 617-622.   DOI: 10.3870/j.issn.1672-8009.2025.06.013 Abstract （54）      PDF （1459KB）（7）       Knowledge map    Save Retinoic acid-induced gene Ⅰ(RIG-Ⅰ),served as a cytoplasmic pattern recognition receptor,is capable of recognizing RNA viruses,and can activate mitochondrial antiviral signaling protein(MAVS)through conformational changes and trigger the TBK1-IRF3/IKK-NF-κB pathway to induce type I interferon(IFN-Ⅰ)production.Mutations in the RIG-I encoding gene DDX58 or excessive activation of RIG-I can lead to the overproduction of inflammatory mediators such as IFN-I,promoting apoptosis and autoantibody formation,resulting in damage to multiple organs including the heart,brain,and kidneys.The cross-disease role of RIG-I in both infectious and non-infectious diseases has gained significant attention in recent years.This article reviews RIG-Ⅰand its roles in systemic lupus erythematosus,tumors,and cardiovascular diseases. Reference | Related Articles | Metrics Select Research Progress on Ferroptosis Associated Mechanisms in Amyotrophic Lateral Sclerosis LI Shujie, QI Yan, SUN Zhitang Journal of Medical Molecular Biology    2025, 22 (6): 623-629.   DOI: 10.3870/j.issn.1672-8009.2025.06.014 Abstract （50）      PDF （2029KB）（11）       Knowledge map    Save Amyotrophic lateral sclerosis(ALS)is a fatal neurodegenerative disease,and the selective death of motor neurons is its prominent pathological feature.The mechanisms triggering the death of ALS neurons are intricate.Currently,there is no effective treatment plan.It is urgent to deeply explore the potential disease mechanisms and search for neuroprotective agents that may delay disease progression,extend survival,and ultimately reduce the disease burden.Ferroptosis is a programmed cell death mode mediated by iron ions,which causes neuronal damage through lipid peroxidation and oxidative stress.Recent studies have revealed that ferroptosis is closely related to the pathological mechanism of ALS and may become a potential therapeutic target.This article reviews the molecular mechanisms of ferroptosis,pathological characteristics of ALS,and potential connections between the two.It also explores the latest advances in clinical trials targeting ferroptosis for the treatment of ALS,with the aim of opening up new avenues for ALS treatment. Reference | Related Articles | Metrics Select Current Application and Recommendations of Artificial Intelligence in Precision Nursing Talent Training LI Wenjing, LI Lingyan, OUYANG Yan, WANG Hanwenxi, HOU Zhixuan, DAI Mengna, GUI Shaozhi, LI Suyun Journal of Medical Molecular Biology    2025, 22 (6): 630-634.   DOI: 10.3870/j.issn.1672-8009.2025.06.015 Abstract （47）      PDF （739KB）（4）       Knowledge map    Save With the rapid development of artificial intelligence technology,it provides new pathways for cultivation of precision nursing professionals.This paper reviews the goals of precision nursing talent development,the advantages and current applications of artificial intelligence in precision nursing education,analyzes the challenges,and proposes development recommendations.It aims to provide reference for the application of artificial intelligence in precision nursing talent training. Reference | Related Articles | Metrics