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31 January 2024, Volume 21 Issue 1
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Mechanism of Fam172a Gene Knockout Exacerbating Non-alcoholic Fatty Liver Disease #br#
LI Mengqi#, WEI Herui#, AN Wen, LOU Jing, HE Lingling, YANG Junru, XIAO Fan, Δ, WEI Hongshan, Δ
2024, 21(1):  1-8.  doi:10.3870/j.issn.1672-8009.2024.01.001
Abstract ( 159 )   PDF (4185KB) ( 94 )  
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ObjectiveTo explore the mechanism of Fam172a gene knockout in enhancing endoplasmic reticulum stress (ERS) induced nonalcoholic fatty liver disease (NAFLD). Methods Mice were intraperitoneally injected with PBS, tunicamycin ( TM), or the NF-κB inhibitor DHMEQ. The hepatic function and hepatic lipid accumulation were then evaluated, and protein levelswere assessed via Western blotting. Results Compared to the control group, the Fam172a - / - -TMgroup had significantly increased levels of serum ALT and AST, along with the increased liver structure damage and lipid accumulation. Additionally, the relative expression levels of GRP78, CHOP,and pNF-κB / NF-κB in liver tissues were significantly up-regulated in the Fam172a - / - -TM group. Furthermore, DHMEQ significantly reduced liver injury, lipid accumulation, and ERS inFam172a - / - mice. Conclusion Fam172a knockout could enhance the ERS-induced NAFLD byactivation of NF-κB pathway.
miR-30b-3p Regulates Sodium Oxalate Induced Apoptosis and Oxidative Stress in HK-2 Cells by Targeting ZNRF1 #br#
YU Dapeng, DING Youpeng, LI Mianzhou, ZHANG Rongyuan,
2024, 21(1):  9-16.  doi:10.3870/j.issn.1672-8009.2024.01.002
Abstract ( 109 )   PDF (3629KB) ( 76 )  
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Objective To explore the effect of miR-30b-3p on HK-2 cell proliferation, apoptosis and oxidative stress induced by sodium oxalate and the mechanism by targeting ZNRF1. Methods HK-2 cells were treated with 0. 2 μmol / L or 0. 6 μmol / L sodium oxalate. miR-30b-3p mimic and miR-30b-3p inhibitor and their corresponding control were transfected into HK-2 cells. The proliferation, invasion and migration of HK-2 cells were detected by CCK-8, transwell and wound-healing assay, respectively. Intracellular ROS was measured by flow cytometry. The activities of LDH, MDA and GSH were detected by ELISA. The expression levels of Bax and Bcl-2 were analyzed by Western blotting. Luciferase gene reporter assay was used to verify the targeting relationship between miR-30b-3p and ZNRF1. The relationship between miR-30b-3p and ZNRF1 was analyzed by RNA immunoprecipitation. Results  Sodium oxalate treatment significantly increased ROS, LDH and MDA levels and decreased GSH levels in HK-2 cells (P< 0. 01). Sodium oxalate also inhibited the proliferation, migration and invasion, and promoted apoptosis of HK-2 cells. miR-30b-3p promoted the effect of sodium oxalate on HK-2 cells. The results of gene target prediction and luciferase assay indicated that ZNRF1 is a direct target of miR-30b-3p in HK-2 cells, and ZNRF1 silencing reversed the effect of miR-30b-3p on sodium oxalate induced HK-2 cell damage. Conclusion miR-30b-3pcan promote the apoptosis and oxidative stress induced by sodium oxalate in HK-2 cells, and inhibitcell proliferation, invasion and migrationvia ZNRF1.

miR-126-5p Inhibits Oxygen-glucose Deprivation / Reperfusion Mediated Apoptosis and Inflammatory Response in HT22 Cells by Targeting TRAF3 #br#
ZHAO Li, ZHAO Lei, XIE Ailing, WANG Yamei, WU Yujuan, TANG Shuang
2024, 21(1):  17-24.  doi:10.3870/j.issn.1672-8009.2024.01.003
Abstract ( 71 )   PDF (2733KB) ( 239 )  
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Objective To explore the effect of miR-126-5p on apoptosis and inflammatory response in mouse hippocampal neuron HT22 cells mediated by oxygen-glucose deprivation / reperfusion (OGD / R) by targeting tumor necrosis factor receptor-associated factor 3 (TRAF3). Methods The OGD / R cell model was established in vitro by simulating ischemia / reperfusion (I / R) injury. The targeting relationship between miR-126-5p and TRAF3 and the effect of miR-126-5p on apoptosis and inflammatory response in HT22 cells were analyzed. Results The level of miR-126-5p inthe OGD / R group was down-regulated while the mRNA and expression levels of TRAF3 were upregulated when compared with those in the control group. The cell survival rate and the Bcl-2 expression level in the OGD / R group were decreased while the lactate dehydrogenase ( LDH) release, the apoptosis rate and the protein expression levels of Bax and cleaved caspase-3 in the OGD / Rgroup were increased when compared with those in the control group (all P< 0. 05). The protein expression levels of TRAF3, Bax and cleaved caspase-3, the LDH release, the apoptosis rate were significantly decreased in the OGD / R + miR-mimic group and the OGD + miR-mimic + pcDNA group while the cell survival rate and the protein expression level of Bcl-2 were increased when compared with those in the OGD / R + mimic-NC group. In addition, the above indicators were elevated in the OGD + miR-mimic + pcDNA-TRAF3 group while the cell survival rate was significantly lowered when compared with those in the OGD/R+mimic-NC group (all P<0.05). Conclusion  miR-126-5p can inhibit the OGD/R-mediated apoptosis of and inflammatory response in HT22 cells by targeting TRAF3, thus playing a protective role on neuronal cells.




miR-200c Regulates Proliferation and Apoptosis of Cervical Cancer Cells via Targeting ZEB1 Expression #br#
FENG Baoju, JIANG Ying, LV Xijun
2024, 21(1):  25-31.  doi:10.3870/j.issn.1672-8009.2024.01.004
Abstract ( 89 )   PDF (1501KB) ( 65 )  
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Objective To study the effect of miR-200c on the proliferation and apoptosis ofcervical cancer cells and its possible mechanism. Methods RT-PCR was used to detect the expression level of miR-200c in 52 cases of cervical cancer tissues and adjacent tissues. The miR-200c mimic or inhibitor was used to transfect cervical cancer cell lines, and the transfection efficiency was verified by RT-PCR. CCK8 assay was used to detect the proliferation activity of transfected cells, while the apoptosis was detected by flow cytometry. The target gene of miR-200c was predicted by bioinformatics analysis, and the dual-luciferase gene reporter assay was applied to verify the targeting relationship. RT-PCR was used to detect the expression level of the target gene in cancer tissuesand adjacent tissues. Pearson correlation analysis between miR-200c and target gene expression wasanalyzed. RT-PCR and Western blotting were used to detect the expression level of target gene incells transfected with siRNA or plasmid. Results The expression level of miR-200c in cervicalcancer tissues was significantly lower than that in adjacent tissues. The proliferation activity of HT3 cells transfected with miR-200c mimics was significantly reduced, and the apoptosis was significantly increased, while the proliferation activity of HeLa cells transfected with miR-200c inhibitors was significantly increased, and the apoptosis of the above cells was significantly reduced. Dual-luciferase gene reporter assay confirmed that ZEB1 is an indicator target of miR-200c, and miR-200c mimics significantly reduced the expression level of ZEB1, while the inhibitor exerted the opposite effect. The expression level of ZEB1 in cervical cancer tissues was significantly higher than that in adjacent tissues, and its expression was significantly negatively correlated with the expression of miR-200c. Knockdown of ZEB1 significantly inhibited the proliferation of HT3 cells and promotedthe apoptosis of cells, while the overexpression of ZEB1 had the opposite effect. Conclusion miR-200c regulates the proliferation and apoptosis of cervical cancer cells by targeting the expression of ZEB1, thereby participating in the occurrence and development of cervical cancer.

Clearance Mechanism of NLRP3 Against Pseudomonas aeruginosa via TLR4 / NF-κB Pathway #br#
LIU Xin, LI Maoxin, YAN Bingjian, XU Zongjie
2024, 21(1):  32-38.  doi:10.3870/j.issn.1672-8009.2024.01.005
Abstract ( 84 )   PDF (1123KB) ( 58 )  
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Objective To investigate the clearance mechanism of NLRP3 against Pseudomonas aeruginosa (PA) based on TLR4 / NF-κB pathway. Methods PA-infected HP-1-induced differentiated macrophages and primary human monocyte-derived macrophages were used for following experiments. NLRP3 and TLR4 were later silenced in macrophages by siRNAs (si-NLRP3 and si-TLR4), and the expression levels of IL-1β and IL-8 in the supernatant were detected by ELISA. The mRNA expression levels of NLRP3 and caspase-1 were detected by RT-PCR. The protein expression levelsof TLR4 and p-NF-κB P65 were detected by Western blotting. Results The levels of IL-1β, IL-8,the mRNA expression levels of NLRP3, caspase-1 and TLR4, and the protein expression level of pNF-κB P65 were significantly increased in the supernatants or cells of the PA-infected THP-1-induced differentiated macrophages and primary human monocyte-derived macrophages hMDMs (P <0. 05). The levels of IL-1β, IL-8, the expression levels of NLRP3, caspase-1 mRNA and TLR4,p-NF-κB P65 protein in the supernatants of the si-NLRP3 and si-TLR4 groups (NLRP3 and TLR4were silenced in THP-1-induced differentiated macrophages and primary human monocyte-derivedmacrophages hMDMs) were significantly reduced when compared with those in the si-NC group (P< 0. 05). The clearance rate was significantly increased in NLRP3 and / or TLR4 silenced PA-infected THP-1 macrophages and primary human monocyte-derived macrophage hMDMs when comparedwith that in the si-NC group (P < 0. 05). Conclusion Silencing NLRP3 increases the clearance of Pseudomonas aeruginosa by macrophages, and the mechanism may be related to the inhibition ofTLR4 / NF-κB signaling pathway activation.

Mechanism of HMGB1 Neutralizing Antibody Inhibiting Pyroptosis and Improving Lung Injury in Mice with Systemic Lupus Erythematosus #br#
LI Mingyuan, MENG Yan, WU Yun
2024, 21(1):  39-44.  doi:10.3870/j.issn.1672-8009.2024.01.006
Abstract ( 143 )   PDF (6502KB) ( 90 )  
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Objective To investigate the effect of neutralizing antibody of high mobility groupprotein 1 (HMGB1) on lung injury in systemic lupus erythematosus (SLE) mice and the underlying mechanism. Methods Thirty MRL / lpr mice were randomly divided into 3 groups: MRL / lprgroup, MRL / lpr + anti-HMGB1 group and MRL / lpr + MCC950 group, with 10 mice in each group, and another 10 wild-type C57BL / 6 mice were taken as the control group. Mice in each group were administered for 4 weeks. Hematoxylin-eosin (HE) staining and Masson staining were used to observe the lung histopathological changes and collagen fiber deposition in each group. The levels of interleukin-1β ( IL-1β), IL-6, IL-18 and tumor necrosis factor-α ( TNF-α) in alveolar lavage fluid of mice in each group were detected by enzyme-linked immunosorbent assay ( ELISA). The fluorescence expression of nucleotide-binding oligomerized domain-like receptor protein 3 (NLRP3) in lung tissues of mice in each group was observed by immunofluorescence staining. The expression levels of HMGB1 and NLRP3, apoptosis-related spect-like protein containing a CARD (ASC) protein, Caspase-1, gasdermin D ( GSDMD) in mice lung tissues were detected by Western blotting. Results The lung tissues in the MRL / lpr group showed serious pathological injury symptoms,the collagen fiber deposition area was significantly increased (P< 0. 05), and the levels of IL-1β,IL-6, IL-18 and TNF-α in alveolar lavage fluid were significantly increased, when compared withthose in the control group (P < 0. 05). In addition, the mean fluorescence intensity of NLRP3 in lung tissues in the MRL / lpr group was significantly increased (P< 0. 05), and the relative proteinexpression levels of HMGB1 and NLRP3, ASC, Caspase-1, GSDMD were significantly up-regulated when compared with those in the control group (P< 0. 05). The lung tissue injuries in the MRL /lpr + anti-HMGB1 group and the MRL / lpr + MCC950 group were significantly improved, and the collagen fiber deposition area was significantly reduced, when compared with those in the MRL / lprgroup (P< 0. 05). In addition, the levels of IL-1β, IL-6, IL-18 and TNF-α in alveolar lavage fluid in the MRL / lpr + anti-HMGB1 group and the MRL / lpr + MCC950 group were significantly decreased (P< 0. 05), the mean fluorescence intensity of NLRP3 in lung tissues was significantly decreased (P < 0. 05), and the relative protein expression levels of HMGB1 and NLRP3, ASC,Caspase-1, GSDMD in lung tissues were significantly down-regulated, when compared with those inthe control group (P< 0. 05). Conclusion HMGB1 neutralizing antibody can ameliorate lung injury in mice with SLE, which may be achieved by inhibiting pyroptosis.


Corosolic Acid Inhibits Excess Proliferation and Induces Apoptosis of Human Ovarian Cancer Cells SKOV-3 #br#
SUN Zhe, WANG Junfeng, LI Huiying, YAO Huixin
2024, 21(1):  45-50.  doi:10.3870/j.issn.1672-8009.2024.01.007
Abstract ( 114 )   PDF (6502KB) ( 158 )  
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Objective To investigate the effect of corosolic acid ( CRA) on the proliferationand apoptosis of human ovarian cancer cells SKOV-3 and its mechanism. Methods Cells were divided into 4 groups: Ctrl group, CRA-10 μmol / L group, CRA-20 μmol / L group, and CRA-50 μmol / L groups, each group was treated with corresponding concentration of CRA. CCK-8 assay was used to measure cell growth. Flow cytometry was used to detect cell apoptosis. The protein expression levels of Ki67, Cyclin D1, CDK6, Bcl-2, Bax, cleaved-caspase-3, cleaved-caspase-9, PI3K, AKT, p-AKT were determined by Western blotting. In addition, the cell line derived xenograft model was established by transplanting the human ovarian cancer cells SKOV-3 in nude mice, the volume of the tumors from the nude mice were measured, the rates of Ki67 or VEGF positive cellswere detected by immunohistochemistry. Results In cytological experiments, the cell growth levels, the Bcl-2 / Bax and p-AKT / AKT ratios, the protein expression levels of Ki67, Cyclin D1, CDK6, PI3K in the CRA groups (10, 20, 50 μmol / L) were decreased significantly, and the cell apoptosis rate, protein expression levels of cleaved-caspase-3 and cleaved-caspase-9 were increased notably, when compared with those in the Ctrl group. In animal experiments, the tumor volume, the rates of Ki67 or VEGF positive cells in the CRA groups (10, 20, 50 μmol / L) were decreased markedly, when compared with those in the Ctrl group. Conclusion Corosolic acid can inhibit the excess proliferation of SKOV3 cells, and induce their apoptosis, the mechanism may related to the inhibition of PI3K / AKT signaling pathway.

Predictive Values of Serum CERP, SF, α-Klotho and FGF-23 in Progression of Albuminuria in Patients with Type 2 Diabetes #br#
ZHANG Qianjin, HU Jin’e, HU Yichuan
2024, 21(1):  51-56.  doi:10.3870/j.issn.1672-8009.2024.01.008
Abstract ( 60 )   PDF (996KB) ( 126 )  
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Objective To analyze the values of serum CERP, SF, α-Klotho and FGF-23 in predicting the progression of albuminuria in patients with type 2 diabetes (T2D). Methods A totalof 120 patients with T2D repeatedly admitted to the Department of Endocrinology of Shuyang Hospital for blood glucose control from June 2020 to May 2022 were selected for the retrospective cohort study. The hospitalization data during the index hospitalization and the readmission were used as the baseline data and follow-up data respectively. Patients were divided into 3 groups: non-albuminuria group, micro-albuminuria group, macro-albuminuria group, according to the albuminuria level of baseline data. The levels of CERP, SF α-Klotho and FGF-23 in patient of different groups were compared. The progression of albuminuria was evaluated according to the follow-up data, and the baseline clinical data and levels of CERP, SF, α-Klotho, FGF-23 between patients with and with out albuminuria were compared. The influencing factors of albuminuria progression were analyzed by logistic regression, and the predictive indicators of albuminuria progression were analyzed by ROCcurve. Results The levels of CERP, SF and FGF-23 were increased and the level of α-Klotho wasdecreased with the increase of the albuminuria level in T2D patients (P< 0. 05). The duration of diabetes in the T2D patients with albuminuria progression was longer than that in the T2D patients without albuminuria progression. The proportions of using metformin and SGLT2 inhibitor (SGLT2i) and the level of α-Klotho in the T2D patients with albuminuria progression were lower than those in the T2D patients without albuminuria progression, and the proportion of hypertension, the levels of FBG, UA, CERP, SF and FGF-23 in the T2D patients with albuminuria progression were higherthan those in the T2D patients without albuminuria progression (P< 0. 05). Logistic regression analysis showed that the elevated levels of CERP, SF and FGF-23 were risk factors for the progression of albuminuria, the use of metformin and SGLT2i and the increase of α-Klotho level were protective factors for the progression of albuminuria. ROC curve analysis showed that the levels of serum CERP, SF, α-Klotho and FGF-23 had predictive values for the development of albuminuria, the sensitivity and specificity by using the combined index in predicting the progression of albuminuriawere both higher than those by using single indexes. Conclusion Increased levels of serum CERP,SF, FGF-23 and decreased level of α-Klotho are related with the development of albuminuria in T2D patients. Those four serum indicators have predictive values for the progression of albuminuria.

Identification of LTBP1 as Biomarker for Prognosis of Gastric Cancer and Its Correlation with Tumor Immune Microenvironment #br#
WANG Xiaorui, WANG Mizhu
2024, 21(1):  57-62.  doi:10.3870/j.issn.1672-8009.2024.01.009
Abstract ( 92 )   PDF (6695KB) ( 81 )  
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Objective To explore the biological functions of latent transforming growth factor beta binding protein 1 (LTBP1) in the occurrence, development, and immune microenvironment ofgastric cancer. Methods The expression level of LTBP1 in gastric cancer was analyzed by using TCGA databases, the results were then validated in the gastric cancer tissues and the para-cancerous tissues. The association between LTBP1 expression level and the clinicopathological variables were analyzed by regression proportional analysis method. Cox regression analysis and Kaplan-Meier plots were used to assess the prognostic value of LTBP1 in gastric cancer. The correlation between the expression level of LTBP1 and the immune cells infiltration was analyzed by TIMER. Immunohistochemical staining was used to detect the expression level of LTBP1 protein in gastric cancer tissues and adjacenttissues. Results LTBP1 was significantly up-regulated in the gastric cancer tissues when comparedwith that in the normal samples. Its expression level was significantly correlated with the pathologic TNM stages. Higher LTBP1 expression indicated poor overall survival (OS) in patients with gastric cancer. We identified that LTBP1 expression had a positive correlation with 3 kinds of immune cells infiltration by TIMER. Immunohistochemical results showed that LTBP1 was significantly overexpressedin gastric cancer tissues. Conclusion LTBP1 can be a potential prognostic biomarker for gastric cancer patients and influences tumor immune microenvironment in gastric cancer.
Effect of Breviscapine on Porphyromonas gingivalis Lipopolysaccharide Induced Injury in Human Gingival Fibroblasts #br#
CHAO Xiaoqin, ZHAO Guoting, DONG Zhenyao, MA Minying, YAO Yizhang
2024, 21(1):  63-68.  doi:10.3870/j.issn.1672-8009.2024.01.010
Abstract ( 80 )   PDF (2632KB) ( 53 )  
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Objective To investigate the effect of breviscapine (BVP) on the Porphyromonasgingivalis lipopolysaccharide ( Pg-LPS, hereinafter referred to as LPS) induced injury in humangingival fibroblasts ( HGFs). Methods HGFs cells were cultured in vitro and divided into 5groups: control group, LPS group, LPS + BVP low-, medium- and high-dose groups. CCK-8 method was used to detect cell proliferation. ELISA method was used to detect the levels of inflammatory factors interleukin-1β ( IL-1β), tumor necrosis factor-α ( TNF-α), interleukin-6 ( IL-6 ) and the activity of superoxide dismutase (SOD). Western blotting method was used to detect the expression levels of cyclin D1, cyclin B1 and apoptosis-related B-cell lymphocytoma-2 ( Bcl-2 ), BCL-2-associated X protein (Bax), Caspase-3 proteins in cells. TBA colorimetric method was used to detect the level of malondialdehyde ( MDA) in cells. DCFH-DA method was used to determinethe level of reactive oxygen species ( ROS) in cells. Results The HGFs cell survival rate, thecell migration rate, the protein expression levels of Cyclin B1, Cyclin D1, Bcl-2 and the SOD activity in the LPS group were significantly decreased when compared with those in the control group (P< 0. 05). The apoptosis rate, the protein expression levels of Bax, Caspase-3, the levels of inflammatory factors TNF-α, IL-1β, IL-6, and the levels of MDA and ROS in the LPS group weresignificantly increased when compared with those in the control group (P< 0. 05). The cell survivalrate, the cell migration rate, the protein expression levels of Cyclin B1, Cyclin D1, Bcl-2 and SOD activity in the LPS + BVP low-, medium-and high-dose groups were significantly increased when compared with those in the LPS group, and the apoptosis rate, the protein expression levels of Bax, Caspase-3, the levels of inflammatory factors TNF-α, IL-1β, IL-6, and the levels of MDA and ROS in the LPS + BVP low-, medium- and high-dose groups were significantly decreased whencompared with those in the LPS group (P< 0. 05). Conclusion BVP can reduce LPS-induced HGFs injury through anti-inflammatory and antioxidant mechanism.

Advances in Development and Function of Peripheral Glial Cells #br#
YU Yue#, DENG Hao#, LIU Simin#, QI Zhihui, YE Zhiming, LIU Mengjie, YAO Maojin
2024, 21(1):  69-76.  doi:10.3870/j.issn.1672-8009.2024.01.011
Abstract ( 156 )   PDF (2077KB) ( 98 )  
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Glial cells are essential components of the central nervous system. There’s growingevidence that they play crucial roles in regulating brain function, supporting synaptic growth, and ensuring the blood-brain barrier remains intact. Furthermore, they are implicated in the development and progression of neurodegenerative conditions like Alzheimer’s and Parkinson’s disease, as well as other central nervous system-related inflammatory diseases. However, research on glial cells in peripheral organs has been under-investigated, and their developmental pathways and physiological functions remain to be elucidated. In this review, our main focus is on the origins and functions of glial cells in peripheral tissues. We also delve into the cellular and molecular processes they’re involved in when it comes to central nervous system diseases, aiming to shed more light on their role outside the brain.
Advances in Novel Compounds and Targets Against Candida albicans #br#
WANG Yuxi, YANG Jing
2024, 21(1):  77-80.  doi:10.3870/j.issn.1672-8009.2024.01.012
Abstract ( 176 )   PDF (728KB) ( 100 )  
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In recent years, fungal infections have been rampant worldwide, affecting approximately hundreds of millions of people annually, with nearly 1. 5 million deaths, posing a significantthreat to human health. Candida albicans is one of the most important pathogens responsible for fungal infections, and it causes invasive candidiasis with a mortality rate of 40 % -50 % . However, the limited variety of available antifungal drugs and the increasing severity of drug resistance make theclinical treatment of Candida albicans particularly challenging. Therefore, it is particularly importantto search for new antifungal compounds and unique molecular targets for antifungal therapy. This review summarizes some novel antifungal compounds with significant potential against Candida albicansand some new antifungal targets in recent years.
Advances in Long Non-coding RNA in Primary Glomerulonephritis #br#
ZHAO Yuanmei, HU Wengang, TAN Xiaohong, ZHANG E, DU Jing
2024, 21(1):  81-85.  doi:10.3870/j.issn.1672-8009.2024.01.013
Abstract ( 92 )   PDF (734KB) ( 64 )  
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Primary glomerulonephritis is a group of common renal disease syndromes, whichcan deteriorate the quality of life of patients and increase the risk of renal disease progression. Long non-coding RNA (lncRNA) is a kind of non-coding regulatory RNA that can regulate a variety of cell biological processes. More and more reports have confirmed that lncRNA is closely related to the occurrence and development of primary nephrotic syndrome. Further researches on the relationship between lncRNA and primary glomerulonephritis are expected to lay a theoretical foundation for finding new biomarkers and therapeutic targets for primary glomerulonephritis.
Emerging Roles of Regulators of G Protein Signaling Proteins in Cancer #br#
ZHANG Xuanhe, YE Qing, ZHANG Shushan
2024, 21(1):  86-92.  doi:10.3870/j.issn.1672-8009.2024.01.014
Abstract ( 120 )   PDF (4430KB) ( 143 )  
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G protein coupled receptors (GPCRs) belong to a superfamily of cell surface receptors, which activate heterotrimeric G proteins that transduce a vast variety of extracellular stimuli, including hormones, ions, organic molecules, and light into the intracellular “effectors” to generate cellular responses. It is widely accepted that GPCR signaling pathways have emerged as the critical mediators for oncogenic signaling. Regulators of G protein signaling ( RGS) proteins are key proteins in GPCR signaling regulations. Many members in the RGS family play pivotal roles in the development of malignant tumors and serve as important targets for cancer diagnosis, treatment and prognosis. This review introduces the structural features, biological effects, and regulatory mechanisms of the RGS family, highlights the recent studies of specific roles of RGS proteins in multiple cancer types, and further explains the general characteristics of RGS in Pan-cancer. In addition, this review summarizes the unique role of RGS in tumor microenvironments as well as the current efforts made on cancer therapy via targeting RGS proteins.