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Journal of Medical Molecular Biology 2024 Vol.21
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Mechanism of
Fam
172
a
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
Journal of Medical Molecular Biology 2024, 21 (
1
): 1-8. DOI: 10.3870/j.issn.1672-8009.2024.01.001
Abstract
(
94
)
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Objective
To explore the mechanism of
Fam
172
a
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
Fam
172
a
- / -
-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
Fam
172
a
- / -
-TM group. Furthermore, DHMEQ significantly reduced liver injury, lipid accumulation, and ERS in
Fam
172
a
- / -
mice.
Conclusion
Fam
172
a
knockout could enhance the ERS-induced NAFLD byactivation of NF-κB pathway.
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miR-30b-3p Regulates Sodium Oxalate Induced Apoptosis and Oxidative Stress in HK-2 Cells by Targeting
ZNRF
1
#br#
YU Dapeng, DING Youpeng, LI Mianzhou, ZHANG Rongyuan,
Journal of Medical Molecular Biology 2024, 21 (
1
): 9-16. DOI: 10.3870/j.issn.1672-8009.2024.01.002
Abstract
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57
)
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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
ZNRF
1.
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
ZNRF
1. The relationship between miR-30b-3p and
ZNRF
1 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
ZNRF
1 is a direct target of miR-30b-3p in HK-2 cells, and
ZNRF
1 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
ZNRF
1.
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miR-
126
-
5
p
Inhibits Oxygen-glucose Deprivation / Reperfusion Mediated Apoptosis and Inflammatory Response in HT22 Cells by Targeting
TRAF
3
#br#
ZHAO Li, ZHAO Lei, XIE Ailing, WANG Yamei, WU Yujuan, TANG Shuang
Journal of Medical Molecular Biology 2024, 21 (
1
): 17-24. DOI: 10.3870/j.issn.1672-8009.2024.01.003
Abstract
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35
)
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Objective
To explore the effect of
miR-
126
-
5
p
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
-
5
p
and TRAF3 and the effect of
miR-
126
-
5
p
on apoptosis and inflammatory response in HT22 cells were analyzed.
Results
The level of
miR-
126
-
5
p
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.
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miR-200c Regulates Proliferation and Apoptosis of Cervical Cancer Cells via Targeting ZEB1 Expression
#br#
FENG Baoju, JIANG Ying, LV Xijun
Journal of Medical Molecular Biology 2024, 21 (
1
): 25-31. DOI: 10.3870/j.issn.1672-8009.2024.01.004
Abstract
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44
)
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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.
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Clearance Mechanism of NLRP3 Against
Pseudomonas aeruginosa
via TLR4 / NF-κB Pathway
#br#
LIU Xin, LI Maoxin, YAN Bingjian, XU Zongjie
Journal of Medical Molecular Biology 2024, 21 (
1
): 32-38. DOI: 10.3870/j.issn.1672-8009.2024.01.005
Abstract
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47
)
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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.
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Mechanism of HMGB1 Neutralizing Antibody Inhibiting Pyroptosis and Improving Lung Injury in Mice with Systemic Lupus Erythematosus
#br#
LI Mingyuan, MENG Yan, WU Yun
Journal of Medical Molecular Biology 2024, 21 (
1
): 39-44. DOI: 10.3870/j.issn.1672-8009.2024.01.006
Abstract
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54
)
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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.
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Corosolic Acid Inhibits Excess Proliferation and Induces Apoptosis of Human Ovarian Cancer Cells SKOV-3
#br#
SUN Zhe, WANG Junfeng, LI Huiying, YAO Huixin
Journal of Medical Molecular Biology 2024, 21 (
1
): 45-50. DOI: 10.3870/j.issn.1672-8009.2024.01.007
Abstract
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57
)
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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 vol
ume, 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.
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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
Journal of Medical Molecular Biology 2024, 21 (
1
): 51-56. DOI: 10.3870/j.issn.1672-8009.2024.01.008
Abstract
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24
)
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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.
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Identification of LTBP1 as Biomarker for Prognosis of Gastric Cancer and Its Correlation with Tumor Immune Microenvironment
#br#
WANG Xiaorui, WANG Mizhu
Journal of Medical Molecular Biology 2024, 21 (
1
): 57-62. DOI: 10.3870/j.issn.1672-8009.2024.01.009
Abstract
(
51
)
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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.
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Effect of Breviscapine on
Porphyromonas gingivalis
Lipopolysaccharide Induced Injury in Human Gingival Fibroblasts
#br#
CHAO Xiaoqin, ZHAO Guoting, DONG Zhenyao, MA Minying, YAO Yizhang
Journal of Medical Molecular Biology 2024, 21 (
1
): 63-68. DOI: 10.3870/j.issn.1672-8009.2024.01.010
Abstract
(
34
)
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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.
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Advances in Development and Function of Peripheral Glial Cells
#br#
YU Yue#, DENG Hao#, LIU Simin#, QI Zhihui, YE Zhiming, LIU Mengjie, YAO Maojin
Journal of Medical Molecular Biology 2024, 21 (
1
): 69-76. DOI: 10.3870/j.issn.1672-8009.2024.01.011
Abstract
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87
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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.
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Advances in Novel Compounds and Targets Against
Candida albicans
#br#
WANG Yuxi, YANG Jing
Journal of Medical Molecular Biology 2024, 21 (
1
): 77-80. DOI: 10.3870/j.issn.1672-8009.2024.01.012
Abstract
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79
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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 albicans
and some new antifungal targets in recent years.
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Advances in Long Non-coding RNA in Primary Glomerulonephritis
#br#
ZHAO Yuanmei, HU Wengang, TAN Xiaohong, ZHANG E, DU Jing
Journal of Medical Molecular Biology 2024, 21 (
1
): 81-85. DOI: 10.3870/j.issn.1672-8009.2024.01.013
Abstract
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43
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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.
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Emerging Roles of Regulators of G Protein Signaling Proteins in Cancer
#br#
ZHANG Xuanhe, YE Qing, ZHANG Shushan
Journal of Medical Molecular Biology 2024, 21 (
1
): 86-92. DOI: 10.3870/j.issn.1672-8009.2024.01.014
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57
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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.
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Comparison of Protein Characteristics of Human WASH468 and WASH465
#br#
ZHENG Aixue, ZHANG Luping, TANG Tuo, LI Ping, HONG Xian, DENG Zhihui, WANG Tao
Journal of Medical Molecular Biology 2024, 21 (
2
): 93-99. DOI: 10.3870/j.issn.1672-8009.2024.02.001
Abstract
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141
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Objective
To investigate the differences between two well recognized WiskottAldrich syndrome protein and SCAR homolog ( WASH) with different sequences.
Methods
Immunofluorescence, immunoprecipitation, and laser micro-irradiation were used to analyze the differences between WASH468 and WASH465 in localization patterns, the interaction with FAM21 or Ku proteins, the recruitment to DNA damage sites and the protein stabilities. To analyze the universality and conservation of the two types of WASH sequences, the WASH protein sequences in various organisms were compared, and the WASH coding sequences in various cell types commonly used forbiological and medical research were detected.
Results
Both WASH exhibited a similar way in localizing to endosome. WASH468 exhibited a stronger interaction with FAM21, and was more stable than WASH465. WASH465 exhibited a stronger interaction with Ku protein, and the recruitment of
WASH465 to DNA damage sites was more robust than that of WASH468. The degree of similarity observed between the sequence of WASH468 in humans and the sequences of WASH in other organisms was significantly greater than that observed with WASH465. Moreover, the coding sequences of WASH in various cell types, which are commonly utilized in biological and medical research, exhibited concordance with the sequence of WASH468.
Conclusion
There are differences in the biological characteristics between WASH468 and WASH465, and WASH468 is significantly more universal and conserved than WASH465. Therefore, WASH468 is the conserved human WASH sequence.
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Role of Circulating Eosinophils Mediated by Plasma SPARC in Gastric Cancer
:
A Multivariable Mendelian Randomization Study and Mediation Analysis
#br#
HAN Zhengxuan, YANG Chaogang, XIONG Hao, XIONG Bin,
Journal of Medical Molecular Biology 2024, 21 (
2
): 100-107. DOI: 10.3870/j.issn.1672-8009.2024.02.002
Abstract
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89
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Objective
East Asia exhibits one of the highest global incidence rates of gastriccancer. The intricate relationship between peripheral blood immune cell counts and the onset and progression of gastric cancer is often obscured by reverse causality and confounders. This study employs Mendelian randomization analysis to mitigate associated biases, aiming to elucidate the causalconnection between peripheral immune cell counts and gastric cancer.
Methods
Both univariateand multivariate Mendelian randomization methods were employed to explore the causal relationship
between diverse immune cell subtypes in peripheral blood and the risk of gastric cancer using data from Genome-wide association studies ( GWAS). Exposure factors included counts of white blood cells, granulocytes, neutrophils, eosinophils, basophils, lymphocytes, and monocytes. The primary approach for univariate Mendelian randomization analysis involved the inverse variance-weighted method. Afterwards, a two-step mediation analysis was conducted to investigate the potential roleof plasma proteins in this process.
Results
Mendelian randomization analysis revealed a causal relationship between lymphocytes (
OR
= 1. 094, 95 %
CI
: 1. 009-1. 185,
P
= 0. 029) and eosinophils (
OR
= 0. 881, 95 %
CI
: 0. 813-0. 955,
P
= 0. 002 ) and the incidence of gastric cancer. Sensitivity analysis corroborated the reliability of these results. Furthermore, the association between decreased eosinophil counts and a reduced risk of gastric cancer persisted in multivariate Mendelian randomization analysis (
OR
= 0. 807, 95 %
CI
: 0. 671-0. 970,
P
= 0. 023). Reverse causality was not significant. The secreted protein acidic and rich in cysteine (SPARC) is an extracellular matrix protein that involves in various cell-matrix interactions and cellular signaling pathways, playing a significant role in tumor development. The mediation analysis of 1 124 plasma proteins suggested that plasma SPARC might mediate the protective effect of eosinophils against gastric cancer(Beta = - 0. 030, 95 %
CI
: - 0. 072-0. 000,
P
= 0. 024).
Conclusion
Mendelian randomizationanalysis establishes eosinophil counts as an independent factor in diminishing the incidence of gastric cancer. Plasma SPARC acts as a mediator in this process, suggesting that circulating eosinophil count and plasma SPARC have the potential to become early clinical indicators and therapeutic targets for gastric cancer. The Mendelian randomization method effectively mitigates biases stemming from reverse causality and psychosocial factors. Nevertheless, additional research is imperative to validate its underlying biological mechanisms.
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Effect of PKM2 Neddylation Modification on Right Ventricular Fibrosis in Pulmonary Hypertension Rats
#br#
GUO Wenyun, WANG Lixia, WANG Jinlin
Journal of Medical Molecular Biology 2024, 21 (
2
): 108-114. DOI: 10.3870/j.issn.1672-8009.2024.02.003
Abstract
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88
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Objective
Exploring the effect of PKM2 neddylation modification on myocardial fibrosis in pulmonary hypertension rats.
Methods
SD rats were randomly divided into 3 groups: control group, model group, and MLN4924 group. Pulmonary arteries were detected by HE staining, and right ventricular fibrosis was detected by Masson staining. Primary cardiac fibroblasts were isolated from rats and the expression of α-Smooth muscle actin (α-SMA) was measured by immunofluorescence assay. The si-NC, si-PKM2, and pcDNA3. 1-PKM2 were transfected into the primary cardiac fibroblasts and the expression levels of PKM2, fibrosis related proteins Collagen Ⅰ , Collagen Ⅲ , MMP2, and MMP9 were detected by Western blotting. Immunoprecipitation assay was used to detect the PKM2 neddylation modification. Real time fluorescence quantitative PCR method was used to detect the mRNA expression level of PKM2 in the rat heart tissues. The degradation of PKM2 protein was detected by Western blotting, and the half-life of PKM2 was determined.
Results
The HE staining results showed that the space between pulmonary arterioles (fibrous layer) and intima (inner transport protein) in the model group was significantly widened and the intermediate layer were
thickened. Masson staining showed that the collagen deposition was increased and the fibrosis was more severe in the model group when compared with those in the control group. The expression level of PKM2 protein in the model group was higher than that in the control group, while there was no significant difference in the mRNA expression level. PKM2 underwent neddylation modification in the right ventricular tissues of pulmonary hypertension rats. Knocking down Nedd8 in cardiac fibroblasts or inhibiting neddylation modification with MLN4924 could downregulate the expression levels of PKM2 and fibrosis related proteins Collagen Ⅰ , Collagen Ⅲ , MMP2, MMP9, etc. , promotingthe degradation of PKM2 protein [ (3. 03 ± 0. 23) - (11. 97 ± 0. 66) h,
t
= - 12. 82,
P
<0. 001] . However, the overexpression of Nedd8 could increase the expression level of PKM2 protein. The degree of right ventricular fibrosis and the expression level of α-SMA protein in theMLN4924 group were lower than those in the model group.
Conclusion
Neddylation modificationenhances the protein stability of PKM2, thereby promoting the process of right ventricular fibrosis inthe rat model of pulmonary arterial hypertension.
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LncHAGLR Promotes Inflammatory Response and Apoptosis of Chondrocytes in Osteoarthritis Rats by Targeting miR-26a and Activation of NF-κB
#br#
MENG Xiaoyuan, Wuerkan Yeerken, WANG Zhigang, MA Le
Journal of Medical Molecular Biology 2024, 21 (
2
): 115-123. DOI: 10.3870/j.issn.1672-8009.2024.02.004
Abstract
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57
)
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Objective
To investigate the effect and potential mechanism of long non-codingRNA HAGLR on the inflammatory response and apoptosis of chondrocytes in rats with osteoarthritis.
Methods
StarBase and luciferase gene reporter assay were used to predict and verify the interaction between lncHAGLR and miR-26a. To investigate the regulatory role of lncHAGLR on miR-26a expression, C518 cells were divided into 4 groups: si-lncHAGLR group, si-NC group, miR-26ainhibitor group, and inhibitor-NC group. Furthermore, to study whether lncHAGLR regulates in
flammation and apoptosis in C518 cells by modulating miR-26a, C518 cells were divided into 5 groups: Control group, IL-1β group, IL-1β + si-NC group, IL-1β + si-lncHAGLR group, and IL-1β + si-lncHAGLR + miR-26a-inhibitor group. Real-time quantitative PCR ( qRT-PCR) was used to analyze the expression levels of lncHAGLR and miR-26a. The proliferation, cytotoxicity and apoptosis of C518 cells were detected by MTT, lactate dehydrogenase (LDH) Kit and flow cytometry (FCM). Western blotting assay was used to detect the protein expression levels of cleavedCASPASE3, NF-κB P65, and phosphorylated NF-κB P65 (P-NF-κB P65). The levels of releasedinflammatory factors (TNF-α and IL-6) were detected by ELISA.
Results
lncHAGLR directly targeted miR-26a. The expression level of lncHAGLR in the IL-1β group was significantly higher than that in the Control group, and the expression level of miR-26a was significantly lower than that inthe Control group (all
P
< 0. 05). In addition, cells in the IL-1β + si-lncHAGLR group had reducedIL-1β-induced chondrocyte inflammation, inhibited apoptosis, increased cell viabilities, decreased release of LDH, inhibited expression of cleaved-CASPASE3, and decreased secretions of TNF-αand IL-6 ( all
P
< 0. 05). Moreover, the expression level of P-NF-κB P65 was decreased (
P
<0. 05). Adding of miR-26a-inhibitor ( IL-1β + si-lncHAGLR + miR-26a-inhibitor group) reversedthe performances of cells in the IL-1β + si-lncHAGLR group (all
P
< 0. 05).
Conclusion
lncHAGLR promotes the inflammatory response and apoptosis of chondrocytes in osteoarthritis rats by inhibiting the activation of NF-κB through targeting miR-26a, suggesting that lncHAGLR may be avaluable therapeutic target for osteoarthritis treatment.
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Correlation Analysis of Serum Asprosin Levels and Elderly Patients with Type 2 Diabetic Nephropathy
#br#
LIU Tian, FAN Jingjing, CHEN Mengnan, GUO Mengyuan, LU Hailong
Journal of Medical Molecular Biology 2024, 21 (
2
): 124-128. DOI: 10.3870/j.issn.1672-8009.2024.02.005
Abstract
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62
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Objective
To analyze the correlation between serum Asprosin levels and elderlytype 2 diabetic nephropathy (DN) to provide clues for the search of new early indicators of DN inclinical practice.
Methods
A total of 183 patients with type 2 diabetes mellitus (T2DM) admittedto our hospital from August 2021 to March 2022 were included for this study. According to whether the patients have DN or not, the patients were divided into 2 groups: the T2DM group alone (85 cases) and the combined DN group (98 cases). Another 50 healthy patients were selected for the control group. The serum Asposin levels in each group was detected and the diagnostic efficacy of Asposin in early DN was analyzed.
Results
Asprosin levels were significantly higher in the T2DMgroup [ (1. 64 ± 0. 41) ng / mL] and the combined DN group [ (2. 45 ± 0. 52) ng / mL] whencompared with that in the control group [ (1. 15 ± 0. 23 ng / mL], and Asprosin level in the combined DN group was higher than that in the T2DM group (
P
< 0. 05). Asprosin level was positively correlated with the values of BUN, Cr, UA, HbA1c, FINS, HOMA-IR, UAER (
P
< 0. 05 ) . The level of Asprosin, HbA1c and UAR were risk factors affecting the occurrence of DN (
P
<0. 05). The area under the curve for the diagnosis of DN by Asprosin combined with UAER was0. 879 (95 %
CI
: 0. 813-0. 974,
P
< 0. 05), the diagnostic specificity was 84. 19 % , and thesensitivity was 94. 57 % .
Conclusion
Elderly DN patients exhibit higher expression of serum Asprosin levels, which may serve as an early diagnostic indicator for the presence of diabetic nephropathy in elderly type 2 diabetes patients.
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Role of CCDC25 Mediated Neutrophil Extracellular Traps in Promoting Proliferation
,
Migration and Invasion of Osteosarcoma Cells
#br#
Muteli Maimaiti, XU Leilei, LI Wenqiang, YAN Feihua
Journal of Medical Molecular Biology 2024, 21 (
2
): 129-134. DOI: 10.3870/j.issn.1672-8009.2024.02.006
Abstract
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68
)
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Objective
To investigate the role and underlying mechanisms of neutrophil extracellular traps ( NETs ) in the proliferation, migration, and invasion of osteosarcomacells.
Methods
A total of 20 osteosarcoma patients and 20 healthy subjects were enrolled. Levels ofPAD4 and H3cit in serum were measured by ELISA. Neutrophils were isolated from peripheral blood of both groups to compare NETs formation. Co-culturing experiments were conducted by incubating NETs with osteosarcoma cells (MG63), with the addition of DNA degrading enzyme DNaseⅠ . The groups included Control, NETs, and NETs + DNase Ⅰ groups. CCDC25 protein expression level was detected using Western blotting, cell proliferation was assessed using CCK-8 assay, and cell migration and invasion were evaluated using Transwell assay. MG63 cells were transfected with si-NC and si-CCDC25, then co-cultured with NETs, cells were then divided into 2 groups: si-NC and siCCDC25 groups. CCDC25 protein expression, cell proliferation, and invasion were assessed as described above.
Results
Compared to healthy subjects, osteosarcoma patients showed elevated levels of PAD4 and H3cit in serum (
P
< 0. 05 ), indicating enhanced NETs formation capaci
ty. Compared to the Control group, the NETs group exhibited elevated CCDC25 protein expressionlevel, increased cell proliferation and cell migration and invasion (
P
< 0. 05). The NETs + DNaseⅠ group showed reduced CCDC25 protein expression level, decreased cell proliferation, cell migration and invasion compared to the NETs group (
P
< 0. 05). The si-CCDC25 group, when compared to the si-NC group, demonstrated decreased CCDC25 protein expression level, cell proliferation, cell migration and invasion (P<0.05).
Conclusion
NETs activate osteosarcoma cell CCDC25 expression through released DNA, thereby promoting tumor cell proliferation, and cell migration and invasion.
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Effect of Sufentanil on Cervical Cancer Cell Cycle and Apoptosis Through Long Non-coding RNA CCAT1
#br#
WEN Xu, PANG Xiaoyi, WEN Yan, WANG Rong, DU Qian, XIAO Song
Journal of Medical Molecular Biology 2024, 21 (
2
): 135-140. DOI: 10.3870/j.issn.1672-8009.2024.02.007
Abstract
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43
)
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)
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Objective
To investigate the molecular mechanisms by which sufentanil affects cervical cancer (CC) cells.
Methods
Real-time quantitative PCR ( RT-qPCR) assay was used todetect the expression level of lncRNA CCAT1 in CC tissues and precancerous tissues, and in the cervical epithelial cells GH329 and CC cell lines (HeLa, CaSki, Siha and C4-1) . Subsequently, CC cells CaSki were randomly divided into 4 groups: blank group, sufentanil group, sufentanil + oe-NC group and sufentanil + CCAT1 group. RT-qPCR assay was then used to examine the expression level of lncRNA CCAT1 in each group. Cell Counting Kit-8 (CCK-8) assay was used to detect the cell proliferation ability. Flow cytometry was used to detect the changes of cell cycle and the cellapoptosis.
Results
lncRNA CCAT1 was highly expressed in CC tissues and the CC cell lines (HeLa, CaSki, Siha and C4-1) when compared with that in the precancerous tissues and that in theGH329 cells respectively (
P
< 0. 01) . The expression level of lncRNA CCAT1 in and the proliferation ability of CaSki cells were significantly decreased (
P
< 0. 01), while the proportion of cells in
the G
0
/ G
1
phase and the apoptosis rate were significantly increased (
P
<0. 01) in the sufentanil groupwhen compared with those in the blank group. The expression level of lncRNA CCAT1 and the proliferation ability of CaSki cells in the sufentanil + oe-CCAT1 group were significantly increased (
P
< 0. 01), while the proportion cells in the G
0
/ G
1
phase and cell apoptosis rate were significantly decreased (
P
<0. 01) when compared with those in the sufentanil + oe-NC group.
Conclusion
Sufentanil could blockthe CC cell cycle by decreasing lncRNA CCAT1 expression in CC cells, ultimately inhibiting the proliferative ability of CC cells and promoting cell apoptosis.
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Sennoside B Inhibits the Proliferation
,
Apoptosis and Invasion of Retinoblastoma HXO-Rb44 Cells via Wnt / β-catenin Pathway
#br#
SUN Mengmeng, CUI Bokun, JIA Meng, RAN Liu, WANG Danrong, FENG Suting, ZHANG Hu, HAO Jianzhang
Journal of Medical Molecular Biology 2024, 21 (
2
): 141-145. DOI: 10.3870/j.issn.1672-8009.2024.02.008
Abstract
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58
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Objective
To investigate the effect of sennoside B on proliferation, apoptosis, invasion and Wnt / β-catenin signaling pathway of retinoblastoma HXO-Rb44 cells.
Methods
HXORB44 cells were treated with different doses (0, 5, 10 and 20 μmol / L) of sennoside B, and the cells were randomly divided into four groups: Control group, sennoside B 5 μmol / L group, sennoside B 10 μmol / L group and sennoside B 20 μmol / L group. Cell viability was detected by MTT assay. Colony formation assay was used to detect the colony formation rate. Cell apoptosis rate was detected by flow cytometry. Cell invasion were detected by Transwell assay. Cell pellet-forming experiment was used to detect the diameters and numbers of cell pellets. The protein expression levels of Cleaved Caspase-3, Caspase-3, MMP-2, MMP-9, SOX2, OCT4, CD44, Wnt1, β-cateninwere detected by Western blotting.
Results
The cell viabilities and colony formation rates in thesennoside B 10 and 20 μmol / L groups were significantly decreased when compared with those in theControl group (
P
< 0. 05), the cell apoptosis rates and cleaved Caspase-3 / Caspase-3 expression levels were significantly increased when compared with those in the Control group (
P
< 0. 05). Thenumbers of invaded cells and the protein expression levels of MMP-2 and MMP-9 were significantlydecreased in the sennoside B 10 and 20 μmol / L groups (
P
< 0. 05), the cell pellet diameters, thecell pellet numbers and the protein expression levels of SOX2, OCT4 and CD44 were significantly
decreased (
P
< 0. 05), and the protein expression levels of Wnt1 and β-catenin were significantlydecreased in the sennoside B 10 and 20 μmol / L groups when compared with those in the Controlgroup (
P
< 0. 05).
Conclusion
Sennoside B can induce apoptosis, inhibit the proliferation, invasion and stem-like characteristics of retinoblastoma HXO-Rb44 cells, and inhibit the activation of Wnt / β-catenin signaling pathway.
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Resveratrol Inhibits Renal Fibrosis and Reduces Kidney Damage Caused by Unilateral Ureteral Obstruction
#br#
ZHAN Hongyi, SONG Yaling, HE Shaolin, ZHOU Yangyang
Journal of Medical Molecular Biology 2024, 21 (
2
): 146-153. DOI: 10.3870/j.issn.1672-8009.2024.02.009
Abstract
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40
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Objective
To investigate the effect of resveratrol on renal fibrosis and kidney damage induced by unilateral ureteral obstruction and its related mechanism.
Methods
Sprague-dawley( SD) rats and NRK-49F fibroblasts were used as experimental subjects for
in vivo
study and
in vitro
validation.
In vivo
, TIF rat model was establish by surgery to induce the unilateral ureteral obstruction in SD rats, and the rats were then randomly divided into 4 groups: sham operation + blankgroup, sham operation + resveratrol group, model + blank group and model + resveratrol group, 12rats in each group.
In vitro
: NRK-49F cells were treated with recombinant TGF-β1 (5 ng / mL) orresveratrol (10 and 100 μmol / L) and randomly divided into 4 groups: control group, TGF-β1 group, TGF-β1 + resveratrol low-dose group and TGF-β + resveratrol high-dose group. Masson’ s staining was used to detect total collagen deposition in the kidney. Immunohistochemical staining was used to detect the expression of E-cadherin, GFAP and Ki67 in the tissues. Immunofluorescence staining was used to detect the expression of Ki67 in cells. Western blotting was used to detect the expression level of Vimentin, N-cadherin, Racl, c-Myc, Bcl-2, Cyclin D1, α-SMA, type I collagen and type Ⅲ collagen, E-cadherin.
Results
Resveratrol could inhibit the excessive depositionof total collagen in kidneys of UUO rats, down-regulate α-SMA-positive myofibroblasts, reduce the
expression of vimentin, type I and type Ⅲ collagen, and inhibit the up-regulation of Rac1, GFAP and down-regulation of N-cadherin. Resveratrol could significantly reduce the ratio of Ki67-positive cells in UUO rats and inhibit the expression level of c-Myc, Bcl-2 and cyclin D1. Resveratrol inhibited the activation of proliferation-related pathway Wnt / β-catenin. The
in vitro
experimentsshowedthat resveratrol treatment could reduce the proliferation of fibroblasts and TECs, thereby inhibiting
TGF-β1-mediated phenotypic transformation and ECM accumulation.
Conclusion
Resveratrol in
hibits the activity of Wnt / β-catenin pathway and the accumulation of myofibroblasts, and reduces
renal tubulointerstitial fibrosis.
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Expressions of miR-144-3p and Its Target Gene
PTEN
in Ovarian Granule Cells and Their Functions in Patients with Polycystic Ovary Syndrome
#br#
SU Jing, ZHANG Rongxue, ZHONG Jixiang, QIU Fenglong, JIA Yuanyuan, XUE Huiying
Journal of Medical Molecular Biology 2024, 21 (
2
): 154-160. DOI: 10.3870/j.issn.1672-8009.2024.02.010
Abstract
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41
)
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Objective
To investigate the expressions of miR-144-3p and its target gene
PTEN
in ovarian granule cells and their functions in patients with polycystic ovary syndrome.
Methods
Twenty patients with PCOS and 20 controls were recruited. Granulosa cells were collected in both groups and the expression level of miR-144-3p in cells was analyzed. The target genes of miR-144-3p were predicted by TargetScan database, and the binding relationship was verified by dual luciferase gene reporter assay. The human ovarian granulosa cells ( KGN) were resuscitated and transfected with miR-144-3p mimic / mimic NC, or miR-144-3p inhibitor / inhibitor NC, or si-PTEN / siRNANC, and were then accordingly divided into 6 groups: miR-144-3p mimic group, mimic NC group, miR-144-3p inhibitor group, inhibitor NC group, si-PTEN and siRNA-NC group. Cell apoptosis was detected by TUNEL assay. RT-PCR and Western blotting method were used to detect the
relative expression levels of miR-144-3p and PTEN.
Results
RT-PCR results showed that the expression level of miR-144-3p in the PCOS group was significantly lower than that in the control group(
P
< 0. 05). Flow cytometry results showed that the apoptosis rate of granulosa cells in the miR-144- 3p mimic group was significantly lower than that in the mimic-NC group (
P
< 0. 05), while the apoptosis rate of granulosa cells in the miR-144-3p inhibitor group was significantly higher than that inthe inhibitor-NC group (
P
< 0. 05).
PTEN
was predicted as the target gene of miR-144-3p by bioinformatics analysis, and the luciferase gene reporter experiments had confirmed that miR-144-3pcould specifically bind to the PTEN-3 ′ UTR and down-regulate the expression level of
PTEN
gene. RT-PCR assay results showed that the expression level of
PTEN
mRNA in the PCOS group was significantly higher than that in the control group (
P
< 0. 05), and was negatively correlated with the expression level of miR-144-3p (
r
= - 0. 91,
P
< 0. 001). The results of qRT-PCR and Westernblotting showed that the mRNA and protein expression levels of PTEN in the miR-144-3p mimicgroup were significantly lower than those in the NC mimic group (
P
< 0. 05), while the mRNA andprotein expression levels of PTEN in the miR-144-3p inhibitor group were significantly higher thanthose in the inhibitor NC group (
P
< 0. 05). Flow cytometry showed that the apoptosis rate of granulosa cells in the si-PTEN group was significantly lower than that in the siRNA-NC group (
P
<0. 05), while the apoptosis rate of granulosa cells in the miR-144-3p inhibitor + si-PTEN group wassignificantly lower than that in the miR-144-3p inhibitor group (
P
< 0. 05).
Conclusion
The expression level of miR-144-3p in ovarian granule cells in PCOS patients is significantly reduced,while the expression level of
PTEN
gene is significantly increased, which may have promoted theapoptosis of ovarian granule cells in PCOS patients.
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Effect of SRPK1 on Malignant Progression of Triple Negative Breast Cancer Cells by Activation of the PI3K / AKT Pathway
#br#
JIANG Li, WANG Huihui, KE Longzhu, LI Gongzhuo, LUO Li
Journal of Medical Molecular Biology 2024, 21 (
2
): 161-165. DOI: 10.3870/j.issn.1672-8009.2024.02.011
Abstract
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60
)
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Objective
To explore the role of SRPK1 and PI3K / AKT signaling pathway in themalignant progression of triple negative breast cancer ( TNBC) cells.
Methods
The expressionlevel of SRPK1 in TNBC tissues and adjacent tissues was detected by immunohistochemistry. TNBCcell line MDA-MB-231 cells were divided into three groups: si
SRPK
1 group, siNC group andLY294002 group. The proliferation ability of MDA-MB-231 cells was detected by MTT assay. Transwell assay was used to analyze the invasion ability of MDA-MB-231 cells. The apoptosis rate of MDA-MB-231 cells was analyzed by flow cytometry. The expression of PI3K / AKT signalingpathway related proteins and SRPK1 protein were detected by Western blotting.
Results
The expression level of SRPK1 was increased in the TNBC tissues when compared with that in the adjacenttissues. The growth rates of MDA-MB-231 cells in the si
SRPK
1 and LY294002 groups were decreased when compared with that in the siNC group (
P
< 0. 05). The numbers of invasive MDA-MB- 231 cells in the si
SRPK
1 and LY294002 groups were significantly decreased (
P
< 0. 05). The apop
tosis rates of MDA-MB-231 cells in the si
SRPK
1 and LY294002 groups were significantly increased (
P
< 0. 05). The protein expression levels of PI3K and AKT in MDA-MB-231 cells were significantly decreased in the si
SRPK
1 and LY294002 groups (
P
< 0. 05).
Conclusion
SRPK1 is highly expressed in TNBC tissues. After inhibiting the expression of SRPK1, the proliferation and invasion ability of TNBC MDA-MB-231 cells are decreased, and the apoptosis rate is increased. This process is related to the regulation of SRPK1 on PI3K / AKT pathway.
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Research Progress on Role of let-7i-5p in Tumor
#br#
OU Yong, DONG Jiaqi, WANG Ban, LI Yuanyuan, WANG Shukai, CHAO Xu
Journal of Medical Molecular Biology 2024, 21 (
2
): 166-170. DOI: 10.3870/j.issn.1672-8009.2024.02.012
Abstract
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47
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let-7i-5p is a member of non-coding small molecule RNA (miRNA), which inhibits tumor growth, proliferation and migration through multiple targets and signaling pathways. It also has the effect of regulating tumor microenvironment to delay cancer progression and improve tumor drug resistance. This article reviews the research progress of the mechanism of let-7i-5p in liver cancer, breast cancer, colon cancer, cervical cancer, nasopharyngeal cancer, kidney cancer and glioblastoma. It is expected to explore the role that let-7i-5p can play as a new tumor marker to provide a new strategy for tumor prevention and treatment.
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Advances in Gene Expression Regulatory Mechanism of
Helicobacter pylori
Virluence Factor CagA
#br#
WANG Mengmeng, YU Mengchao, WANG Lili, ZHAO Zhenyu, DONG Quanjiang
Journal of Medical Molecular Biology 2024, 21 (
2
): 171-175. DOI: 10.3870/j.issn.1672-8009.2024.02.013
Abstract
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88
)
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About half of the global population has been found to be infected with
Helicobacter pylori
(
H
.
pylori
)
, with particularly high rates in developing countries. Currently,
H
.
pylori
infection has been listed as a high-risk factor for the development of gastric cancer. The pathogenesis of
H
.
pylori
infection is believed to be associated with complex interactions between environment factors, host susceptibilities, and bacterial pathogenicity. Therefore, this article reviews the molecularmechanism of the regulation of
Helicobacter pylori
independent factor
cagA
expression, in order tobetter understand the pathogenicity of
cagA
and to provide a theoretical reference for the future prevention and treatment of diseases caused by
H
.
pylori
.
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Research Progress on Glucocorticoids Induced Dysfunction of Trabecular Meshwork
#br#
REN Jing, DUAN Shichao, CUI Huiling, WANG Di, ZHAO Rumeng, LI Haijun
Journal of Medical Molecular Biology 2024, 21 (
2
): 176-181. DOI: 10.3870/j.issn.1672-8009.2024.02.014
Abstract
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54
)
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Glucocorticoids (GCs) could induce the morphological changes and dysfunction oftrabecular meshwork tissues. The changes in the trabecular meshwork tissues of the glucocorticoids ( GCs) induced glaucoma is similar with those of the primary open angle glaucoma ( POAG). However, the pathogenesis of POAG is still unclear, elucidating how GCs induce morphological changes of trabecular meshwork and the increase of aqueous humor outflow resistance is beneficial for exploring the pathogenesis of POAG. The effects of GCs on trabecular meshwork are summarized in this review.
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Advances in Mechanism of Hypoxia in the Progression and Treatment Tolerance of Lung Cancer
#br#
CHEN Keming, YU Wanjun, WANG Huaying, FU Zhongming
Journal of Medical Molecular Biology 2024, 21 (
2
): 182-186. DOI: 10.3870/j.issn.1672-8009.2024.02.015
Abstract
(
80
)
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Hypoxia is an intrinsic feature of lung cancer. It affects the metabolism, proliferationand migration of lung cancer through genomic and proteomic regulation, and up-regulates the tolerance of lung cancer to radiotherapy and induces the resistance of lung cancer to chemotherapy and immunotherapy through complex mechanisms, which make it an important factor leading to the poor prognosis of lung cancer. This article reviews the mechanism of hypoxia in the drug resistance of lung cancer and its potential application as a therapeutic target in the clinical treatment of lung cancer.
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Study of Mutual Regulation between TRIM21 and TRIM8 in Glioma U251 Cells
#br#
WANG Lin∗ , LIU Xuemei∗ , LI Hui, HUANG Aixue, ZHAO Yuechao, XIAO Can, GAO Bo, SHAO Ningsheng
Journal of Medical Molecular Biology 2024, 21 (
3
): 187-195. DOI: 10.3870/j.issn.1672-8009.2024.03.001
Abstract
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Objective
To explore the mutual regulation between TRIM21 and TRIM8 in glioma U251 cells.
Methods
TRIM21 and TRIM8 were overexpressed or knocked down respectively in U251cells, and their protein and mRNA expression levels were detected by Western blotting and RT-PCR respectively. Immunofluorescence experiment was used to analyze the subcellular localization of TRIM21 and TRIM8. The interaction between TRIM21 and TRIM8 was verified by immunoprecipitation experiment. The ubiquitination modification of TRIM21 or TRIM8 was analyzed by intracellular ubiquitination experiment. Protease inhibitor MG-132 was used to inhibit protease activity. U251 cell apoptosis was detected by flow cytometry assay.
Results
TRIM21 and TRIM8 could negatively regulate each other on theprotein level in U251 cells which resulted in cell apoptosis inhibition. Mechanism study showed that there was an interaction between TRIM21 and TRIM8 in U251 cells, that interaction furtherly activated ubiquitin-proteasome-dependent degradation pathway through ubiquitination.
Conclusion
Negatively mutualregulation between TRIM21 and TRIM8 is achieved through ubiquitination modification, following ubiquitin-proteasome-dependent degradation. Our results suggested that it is important to maintain a balance between TRIM21 and TRIM8 on protein level, that is, three might exist an E3 ubiquitin ligase protein homeostasis. The homeostasis disorder will be highly related to the tumorigenesis.
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Role of RIPK3 in LPS / D-GalN Induced Acute Liver Failure
#br#
YU Qian, BIAN Shu, ZHANG Yuting, ZHAO Sai, LIU Liangming
Journal of Medical Molecular Biology 2024, 21 (
3
): 196-202. DOI: 10.3870/j.issn.1672-8009.2024.03.002
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137
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Objective
To study the role of receptor-interacting protein kinase 3 ( RIPK3) in acute liver failure induced by lipopolysaccharide / D-galactosamine (LPS / D-GalN).
Methods
SPFgrade male BALB / c mice were randomly divided into 3 groups (
n
= 5). The ALF animal model wasestablished by intraperitoneal injection of LPS combined with D-GalN. One hour before intraperitoneal drug injection, the mice were pretreated with intravenous injections of 0. 1 % DMSO and the RIPK3-specific antagonist GSK872 (dissolved in 0. 1 % DMSO), respectively. The degree of liver injury was assessed by blood biochemical tests and histological changes in the liver tissue. PCR was used to detect the expression levels of mRNA, while Western blotting and immunohistochemistrywas used to detect the expression levels of proteins.
Results
Animal experimental results showedthat LPS / D-GalN-challenged mice exhibited significant inflammatory hemorrhagic necrotic damageand increased infiltration of F4 / 80
+
cells in liver tissues, and a notable elevation of ALT and AST levels in blood (both
P
< 0. 01) when compared with the control. In addition, the mRNA levels of
F
4
/
80,
Mcp-
1,
Tnf-α
,
Il-
6,
Ripk
3 and
Mlkl
, as well as the levels of RIPK3 protein and pMLKL / MLKL protein ratio, were all upregulated in liver tissues in comparison with the controlgroup, with all differences being statistically significant ( all
P
< 0. 05). Compared to the mice in
the LPS / D-GalN group, the GSK872-pretreated mice displayed a marked reduction in the degree ofliver inflammatory injury, a significant decrease in the infiltration of F4 / 80
+
cells in the liver, anda substantial decline in serum ALT and AST levels (both
P
< 0. 01). The mRNA levels of
F
4
/
80,
Mcp-
1,
Tnf-α
,
Il-
6,
Ripk
3, and
Mlkl
as well as the levels of RIPK3 protein and p-MLKL / MLKLprotein ratio, were all downregulated in liver tissues, with all differences being statistically significant (all
P
< 0. 05).
Conclusion
The RIPK3 inhibitor GSK872 can significantly block the expression of RIPK3 in LPS / D-GalN-induced ALF in mice, mitigate liver tissue damage and inflammatorycell infiltration, and suppress the expression of necroptosis-related proteins. This suggests thatRIPK3 might promote the pathogenesis of ALF by influencing the molecules of the hepatic necroptotic apoptosis pathway.
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All-trans Retinoic Acid Alleviates Endoplasmic Reticulum Stress and Improves Isoproterenol Induced Myocardial Fibrosis and Myocardial Remodeling in Rats
#br#
WEI Junping, MENG Qingwen, LIN Daofei, LIN Yanzai, FU Dajia
Journal of Medical Molecular Biology 2024, 21 (
3
): 203-210. DOI: 10.3870/j.issn.1672-8009.2024.03.003
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33
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Objective
To investigate the effects of all-trans retinoic acid (ATRA) on myocar
dial fibrosis and myocardial remodeling induced by isoproterenol (ISO) in rats, and to analyze itsmechanism.
Methods
The rats were randomly divided into 4 groups: control group, ISO group,ATRA + ISO group, 4-phenylbutyric acid (4-PBA) + ISO group, with 10 rats in each group. Rats in the ATRA + ISO group and the 4-PBA + ISO group were administrated with ATRA and 4-PBA through intraperitoneal injection respectively. Rats in the ISO group, the ATRA + ISO group and the 4-PBA + ISO group were administrated with ISO through subcutaneous injection on the back. The left ventricular internal diameter in diastole ( LVIDd), left ventricular internal diameter in systole ( LVIDs), left ventricular ejection fraction (EF) and fractional shortening (FS) were detected by cardiac ultrasound. The body weight, whole heart mass and left ventricular mass of rats were weighed, and the whole heart mass index ( HMI) and left ventricular mass index ( LVMI) were calculated. The level of serum N-terminal pro B type natriuretic peptide ( NT-proBNP) was determined by ELISA. HE staining and Masson staining were used to observe the histopathological changes and the degree of collagen fibrosis in rat myocardial tissues, respectively. The protein expression levels of G protein-coupled receptor 78 (GRP78), C / EBP homologous protein (CHOP), protein kinase R-like endoplasmic reticulum kinase (PERK), phosphorylated eukaryotic translation initiation factor 2α (p-eIF2α), and transforming growth factor-β1 (TGF-β1), α-smooth muscle actin (α-SMA), Collagen-I and Collagen-Ⅲ in myocardial tissues were determined by Western blotting.
Results
When compared with those in the control group, the EF and FS in the ISO group were significantly decreased (
P
< 0. 05), the LVIDd, LVIDs, HMI and LVMI were significantly increased (
P
< 0. 05), the level of serum NT-proBNP was significantly increased (
P
< 0. 05), thepathological injury of myocardial tissues was observed, the areas with collagen fiber had significantlyincreased (
P
< 0. 05), the protein expression levels of GRP78, CHOP, PERK, P-EIF2α, TGF-β1, α-SMA, Collagen Ⅰ and Collagen Ⅲ in the myocardial tissues were significantly up-regulated(
P
< 0. 05). When compared with those in the ISO group, the EF and FS in the ATRA + ISO group and the 4-PBA + ISO group were significantly increased (
P
< 0. 05), the LVIDd, LVIDs, HMI and LVMI were significantly decreased (
P
< 0. 05), and the level of serum NT-proBNP was significantly decreased (
P
< 0. 05), the degree of myocardial injury was significantly reduced, the area with collagen fiber had significantly reduced (
P
< 0. 05 ), and the protein expression levels ofGRP78, CHOP, PERK, P-EIF2α, TGF-β1, α-SMA, Collagen Ⅰ and Collagen Ⅲ in the myocardial tissue were significantly down-regulated (
P
< 0. 05).
Conclusion
ATRA can alleviate ISOinduced myocardial injury and fibrosis, inhibit myocardial remodeling and improve cardiac function through the inhibition of endoplasmic reticulum stress response.
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HDAC3 Inhibitor RGFP966 Alleviates Endometrial Fibrosis by Regulation of AIM2 Inflammasome and EMT through TGF-β1 / SMAD3 / STAT-1 Signaling Pathway
#br#
LU Jianjun, ZHANG Xinyue
Journal of Medical Molecular Biology 2024, 21 (
3
): 211-216. DOI: 10.3870/j.issn.1672-8009.2024.03.004
Abstract
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46
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Objective
To investigate the molecular mechanisms of HDAC3 inhibitor RGFP966 in alleviating endometrial fibrosis.
Methods
A total of 18 female SD rats (6-8 weeks) were randomly divided into 3 groups: Control group, IUA Model group (intrauterine adhesion rat Model), and RGFP966 Treatment group ( IUA model group rats were treated with HDAC3 inhibitor RGFP966), with 6 rats in each group. IUA rat model was established. ELISA was used to determine the levels of the serum inflammatory cytokines TNF-α, IL-1β and IL-6. qPCR was used to determine the relative mRNA expression levels of EMT markers E-cadherin, N-cadherin, α-SMA and Vimentin. Western blotting was used to determine the protein expression levels of TGF-β1, SMAD3, phosphorylated STAT-1, STAT-1, AIM2, IL-18, cleaved IL-1β and IL-1β.
Results
The walls of uterine horn in the IUAModel group were thinner, the levels of serum inflammatory cytokines TNF-α, IL-1β and IL-6 were increased when compared with those in the Control group (
P
<0. 05). The relative expression levels of Ecadherin mRNA were decreased, while the relative expression levels of N-cadherin, α-SMA and Vimentin mRNA were increased (
P
< 0. 05). The expression levels of TGF-β1, SMAD3, p-STAT-1 were enhanced (
P
< 0. 05). And the expression levels of AIM2, IL-18, cleaved IL-1β were increased (
P
<
0. 05). The above indicators were partially reversed in RGFP966 Treatment group when compared withthose in the IUA Model group (
P
<0. 05). No significant differences in the expression levels of STAT-1and IL-1β were seen among the three groups (
P
>0. 05).
Conclusion
HDAC3 inhibitor RGFP966 canalleviate endometrial fibrosis by down-regulating TGF-β1/ SMAD3/ STAT-1 signaling pathway to inhibitAIM2 inflammasome activation and EMT.
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Effect of Insulin-like Growth Factor 1 Gene Transfected Bone Marrow Mesenchymal Stem Cells on Fracture Healing and Angiogenesis
#br#
WANG Gui, LI Zuncheng, LIU Jingxin, CHEN Yuxing
Journal of Medical Molecular Biology 2024, 21 (
3
): 217-223. DOI: 10.3870/j.issn.1672-8009.2024.03.005
Abstract
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28
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Objective
To investigate the effect of insulin-like growth factor 1 (
IGF
1) genetransfected bone marrow mesenchymal stem cells (BMSCs) on fracture healing and angiogenesis inrats.
Methods
The rat femoral fracture model was established, and the BMSCs with or without
IGF
1 gene transfection were used to treat the rats. X-ray imaging system and micro-CT scanner wereused to observe the fracture healing. HE staining was used to observe the histopathological changes offemur. Immunofluorescence staining was used to observe the expression of vascular endothelial marker CD31. Western blotting was used to detect the expression levels of bone morphogenetic protein 2( BMP-2 ), osteopontin ( OPN ), osteocalcin ( OCN ), vascular endothelial growth factor(VEGF) and angiopoietin-1 ( Ang-1).
Results
When compared with those in the model group,the fracture lines of the rats in the BMSC group and the IGF1-BMSC group were blurred and the formation of healing callus was observed, the values of BMD and BV / TV were increased (
P
< 0. 05), the value of Tb. N was increased (
P
< 0. 05), the value of Tb. Sp was decreased (
P
< 0. 05), theCD31 fluorescence expression was enhanced, the relative protein expression levels of BMP-2,OPN, OCN, VEGF and Ang-1 were all up-regulated (
P
< 0. 05). When compared with those inthe BMSC group, the fracture line of rats in the IGF1-BMSC group was almost disappeared, andthe healing effect was better, the values of BMD and BV / TV were increased (
P
< 0. 05), the value of Tb. N was increased (
P
< 0. 05), the value of Tb. Sp was decreased (
P
< 0. 05), and CD31
fluorescence expression was stronger in the IGF1-BMSC group, the relative protein expression levelsof BMP-2, OPN, OCN, VEGF and Ang-1 were further up-regulated (
P
< 0. 05).
Conclusion
IGF
1 gene transfection with BMSC can effectively promote femoral fracture healing and acceleratevascular formation in rats, and the effect is better than that of BMSC alone.
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Expressions of CLEC1B
,
DKK1 and DRD4 in Primary Hepatic Cancer Tissues and Their Clinical Significance
#br# #br#
DAI Yunlong, HUANG Jiwei
Journal of Medical Molecular Biology 2024, 21 (
3
): 224-230. DOI: 10.3870/j.issn.1672-8009.2024.03.006
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46
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Objective
To analyze the expression and clinical significance of C-type lectin domain family 1 member B (CLEC1B), Dickkopf 1 (DKK1) and dopamine receptor D4 (DRD4)in primary hepatic cancer ( PHC) tissues.
Methods
A retrospective study was conducted among138 patients who underwent liver cancer resection at West China Hospital of Sichuan University fromJanuary 2022 to January 2023 and were diagnosed with PHC by postoperative pathology. Paraffin-embedded specimens of the patients’cancer tissues and adjacent tissues were collected to analyze thedifferences in the expression of CLEC1B, DKK1 and DRD4, and their relationship with clinicopathological parameters. Pearson method was used to analyze the correlation among CLEC1B,DKK1, and DRD4.
Results
The expression levels of CLEC1B and DRD4 in the liver cancer tissues were lower than those in the adjacent tissues. The expression level of DKK1 protein in the livercancer tissues was significantly higher than that in the adjacent tissues (
P
< 0. 05). The above threeproteins were mainly distributed in the cytoplasm. Low expression of CLEC1B were found in 97 cases(70. 29 % ), high expression of DKK1 in 91 cases (65. 94 % ), and low expression of DRD4 in78 cases (56. 52 % ). The low expression of CLEC1B in PHC patients was closely related to thepreoperative AFP level, vascular invasion, distant metastasis, and tumor bleeding (
P
< 0. 05).
The high expression of DKKI was closely related to the preoperative AFP level, BCLC Kinki staging, tumor number, and tumor size (
P
< 0. 05). The low expression of DRD4 was closely related tothe preoperative AFP level, tumor number, tumor size, satellite nodule, and vascular invasion(
P
< 0. 05). Pearson correlation analysis found that the expression levels of CLEC1B, DRD4 and DKK1 in PHC patients were negatively correlated (
r
= - 0. 809,
r
= - 0. 774,
P
< 0. 001). The expression levels of CLEC1B and DRD4 were positively correlated (
r
= 0. 748,
P
< 0. 001 ).
Conclusion
CLEC1B and DRD4 are lowly expressed in the PHC tissues, and DKK1 is highly expressed, and their expression changes are all related to the clinicopathological parameters. CLEC1B, DKK1, and DRD4 may be involved in the occurrence and development of PHC. Therefore, they are worthy of detection.
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Formononetin Inhibits Proliferation
,
Migration and Invasion of Esophageal Carcinoma Cells by HNF4A
#br#
ZHOU Jincai, ZANG Ting , LI Zhao , YANG Zhao , LI Wenhai
Journal of Medical Molecular Biology 2024, 21 (
3
): 231-238. DOI: 10.3870/j.issn.1672-8009.2024.03.007
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29
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Objective
To analyze the mechanism of formononetin on inhibiting the proliferation, migration and invasion of esophageal carcinoma (EC) cells by hepatocyte nuclear factor 4α(HNF4A).
Methods
It was concluded by network pharmacology analysis that HNF4A might beone of the targets of formononetin. The expression level of HNF4A was closely related to clinical phenotypes of EC. EC109 and KYSE510 were treated with different concentrations of formononetin. The relative survival rate of cells was detected by CCK8. The cells proliferation was detected by CCK-8. The cancer cells were cultured by cells cloning assay. The number of colony cells before and afterformononetin treatment was detected. The migration and invasion of EC109 and KYSE510 cells before and after formononetin treatment were detected by transwell assay. Nude mice were subcutaneously injected with tumor cells and treated with formononetin to observe the changes in volume andweight of xenograft tumors. The expression level of Ki67 protein in xenograft tissues was detected byimmunohistochemistry. The effect of formononetin on the expression of
HNF
4
A
gene were detected byWestern blotting. EC109 and KYSE510 cell lines with stable overexpression of HNF4A were constructed and treated with formononetin to observe the effect on the expression of HNF4A.
Results
After formononetin treatment, the relative survival rates of EC109 and KYSE510 cells were significantly decreased (
P
< 0. 05). Compared with that of cells without formononetin treatment, the relative survival rate of cells was significantly decreased after treated with formononetin (≥150 μmol / Lfor EC109 cell line, and ≥ 120 μmol / L for KYSE510 cell line) (
P
< 0. 05). The proliferation,migration and invasion of EC109 and KYSE510 cells in the formononetin group was significantly decreased when compared with those in the control group (
P
< 0. 05). The volume and weight of xenograft tumors were significantly decreased in the formononetin group (
P
< 0. 05), and the expression level of Ki67 protein was significantly lower than that in the control group (
P
< 0. 05). The effect offormononetin on the down-regulation of HNF4A protein was dependent on the concentration and time of the treatment. HNF4A overexpression could promote cells proliferation, invasion and migrationwhich were inhibited by formononetin (
P
< 0. 05).
Conclusion
formononetin can inhibit the proliferation, migration and invasion of EC cells by regulation of HNF4A.
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Effect of miR-592 on Migration
,
Invasion and Autophagy of Renal Cell Carcinoma via Targeting PRDM5
#br#
LI Shunlai, SONG Xiaolin, JIANG Tingqi, WANG Wenzhen
Journal of Medical Molecular Biology 2024, 21 (
3
): 239-246. DOI: 10.3870/j.issn.1672-8009.2024.03.008
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29
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Objective
To explore the effect of miR-592 on the migration, invasion and autophagy of renal cell carcinoma ( RCC) via targeting PR domain zinc finger protein 5 ( PRDM5).
Methods
RT-qPCR and Western blotting were used to detect the expression levels of miR-592 andPRDM5 mRNA and protein in RCC tissues and cells. A498 and 786-O cells were divided into 4groups: anti-miR-NC group, anti-miR-592 group, anti-miR-592 + si-NC group and anti-miR-592 + si-PRDM5 group. RNA immunoprecipitation (RIP) was used to determine the combination of miR-592 and PRDM5. CCK-8, wound-healing assay and transwell test were used to analyse the cell proliferation, migration and invasion. Transmission electron microscopy was used to observe the autophagosome formation. Western blotting was used to detect the expression levels of PRDM5, matrix metalloproteinase ( MMP ) -2, MMP-9, Beclin1, microtubule-associated protein 1 light chain 3( LC3) Ⅱ / Ⅰ . Nude mice model of transplanted tumors was established to analyze the effect of knocking down miR-592 on the growth of transplanted tumors.
Results
PRDM5 mRNA and protein expression levels in the RCC tissues and cells were decreased (
P
< 0. 05). After knocking down the expression of miR-592, the cell
A
450
value, the number of migrated and invaded cells, the expression levelsof MMP-2 and MMP-9 were decreased, while the number of autophagosomes, the expression levels ofBeclin1 and LC3 II / I were increased (
P
< 0. 05). Knocking down the expression of PRDM5 could par
tially reverse the effect of miR-592 knock-down on cell proliferation, invasion and autophagy (
P
<0. 05). Knocking down the expression of miR-592 could inhibit the growth of transplanted tumors innude mice (
P
<0. 05).
Conclusion
miR-592 promotes the proliferation, invasion and migration ofRCC cells, and inhibits autophagy by targeting the expression of PRDM5.
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Mechanism of LINC00319 Regulating PENK / PI3K / AKT Signaling Pathway in Osteosarcoma
#br#
XIA Fei, ZHANG Haiping
Journal of Medical Molecular Biology 2024, 21 (
3
): 247-253. DOI: 10.3870/j.issn.1672-8009.2024.03.009
Abstract
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39
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Objective
To explore the mechanism of LINC00319 regulating PENK / PI3K / AKTsignal pathway in osteosarcoma (OS).
Methods
The expression levels of LINC00319 and PENK inthe peripheral blood RNAs from OS patients and non-OS patients were detected using qPCR, and the correlation between LINC00319 and PENK expression were analyzed. Knockdown or overexpression of LINC00319 were performed in the MG63 cells, and the mRNA and protein expression levels of PENK were detected using qPCR and Western blotting methods, respectively. The mouse OS transplanted tumor model was established and mice were divided into 2 groups: shNC group and shLINC00319 group. The tumor weight was measured, and the expression levels of PENK, AKT, p-AKT, and PI3K in the tumor tissues were detected through immunohistochemistry experiments. MG63 cells were divided into 3 groups: shNC group, shLINC00319 group, shLINC00319 + shPENK group. Cell proliferation was detected by EdU. Cell invasion was detected via transwell method. The protein expression levels of AKT, p-AKT, and PI3K were detected using Westernblotting.
Results
The expression level of LINC00319 was higher in the peripheral blood of OS patients, and the expression level of PENK was lower when compared to those in the peripheral blood
of non-OS patients. The expression level of PENK was negatively correlated with the expression level of LINC00319. After knocking down LINC00319, PENK mRNA and protein levels were upregulated, while overexpression of LINC00319 resulted in decreased expression level of PENK mRNA and protein. Compared to mice in the shNC group, mice in the shLINC00319 group showed decreased tumor weight, unchanged expression level of AKT protein in tumor tissues, and deceased expression levels of p-AKT, PI3K protein. Compared to cells in the shNC group, MG63 cells in the shLINC00319 group showed decrease abilities in cell proliferation and invasion, the expression levels of p-AKT and PI3K proteins were decreased in the shLINC00319 group as well. Cells in the shLINC00319 + shPENK group showed increase abilities in cell proliferation and invasion, and the expression levels of p-AKT and PI3K proteins were increased when compared to those in theshLINC00319 group.
Conclusion
LINC00319 is highly expressed in the peripheral blood of OS patients, while PENK is lowly expressed in the peripheral blood of OS patients, and their expression levels are negatively correlated. LINC00319 promotes OS cell proliferation and invasion by inhibiting PENK levels and activating the PI3K / AKT signaling pathway.
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Effect of Blocking PI3K / Akt / mTOR Signaling Transduction on Leukemia HL-60 Cells
#br#
GUO Chen, TANG Jing
Journal of Medical Molecular Biology 2024, 21 (
3
): 254-258. DOI: 10.3870/j.issn.1672-8009.2024.03.010
Abstract
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26
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Objective
To investigate the effect of blocking PI3K / Akt / mTOR signaling on leukemia cells.
Methods
Acute myeloid leukemia cell line HL-60 was selected, cells were randomly divided into 4 groups: blank control group, low concentration group, medium concentration group and high concentration group. Cells in the blank control group was given normal saline, cells in the low concentration group, medium concentration group and high concentration group were treated with 10, 25 and 50
P
mol / L PI3K / Akt / mTOR signaling blocker GDC-0349. CCK-8 method was used to detect the cell proliferation. Cell apoptosis was detected by flow cytometry, and the expression level of PI3K / Akt / mTOR and apoptosis related proteins were detected by Western blotting.
Results
Compared with those in the low and medium concentration groups, the absorbance ratios (
A
values) of cells in the high concentration group at 24, 48 and 72 h time-points were significantly lower (
P
< 0. 05). The apoptosis rates of cells in the low, medium and high concentration groups were significantly higher than that of cells in the blank control group (
P
< 0. 05), and theapoptosis rate of cells in the high concentration group was significantly lower than those of cells inthe low and medium concentration groups (
P
< 0. 05). The relative expression levels of P110, Aktand mTOR in the high concentration group were significantly lower than those in the blank controlgroup, low and medium concentration groups (
P
< 0. 05). The relative expression levels of Bcl2 andCaspase3 proteins in the low, medium and high concentration groups were significantly lower thanthat in the blank control group (
P
< 0. 05). The relative expression levels of Bcl2 and Caspase3 in the high concentration group were significantly lower than those in other groups (
P
< 0. 05).
Con
clusion
Blocking PI3K / Akt / mTOR signaling can inhibit the proliferation and promote the apoptosis of HL-60 cells.
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Expressions of miRNA-218 and miRNA-21 in Gastric Cancer Patients with
Helicobacter pylori
Infection and Their Clinical Significance
#br#
ZOU Ling, ZHANG Heng, WU Jian, LIN Wei, CHEN Xin
Journal of Medical Molecular Biology 2024, 21 (
3
): 259-263. DOI: 10.3870/j.issn.1672-8009.2024.03.011
Abstract
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29
)
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Objective
To explore expressions of miRNA-218 (miR-218) and miR-21 in gastric cancer related to
Helicobacter pylori
(Hp) infection and their clinical significance.
Methods
A total of 104 patients with gastric cancer undergoing surgical resection were enrolled. The relationship between miR-218, miR-21 and clinicopathological factors and postoperative recurrence was analyzed.
Results
The expression Level of miR-218 was lower in the Hp-positive group than in theHp-negative group, while the expression level of miR-21 and the 2-year recurrence rate were higherin the Hp-positive group (
P
< 0. 05). The expression level of miR-218 was lower in the gastric cancer tissues than in the para-carcinoma tissues, while the expression level of miR-21 was higher in thegastric cancer tissues (
P
< 0. 05). The expression levels of miR-218 and miR-21 were correlated withthe differentiation degree, TNM staging, depth of tumor invasion, lymph node metastasis and progression-free survival rate, which were of high predictive value for the 2-year recurrence situation after surgery.
Conclusion
The expression levels of miR-218 and miR-21 are different between gastric cancer patients with or without Hp-infection. The abnormal expressions of miR-218 and miR-21 are related with the clinicopathological factors and prognosis of gastric cancer patients with Hp infection.
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GSK484 Inhibits Neutrophil Extracellular Traps Formation and Inflammatory Response in Ankylosing Spondylitis
#br#
LI Rulin, DU Zhuangwen, WANG Enliang
Journal of Medical Molecular Biology 2024, 21 (
3
): 264-269. DOI: 10.3870/j.issn.1672-8009.2024.03.012
Abstract
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33
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Objective
To investigate the effect of GSK484 on neutrophil extracellular traps(NETs) formation and inflammatory response in ankylosing spondylitis (AS) and its related mechanisms.
Methods
The levels of PAD4, H3cit, IL-1β, IL-6, and the formation of NETs were assessedin peripheral blood from AS patients and healthy subjects. Thirty Balb/ c mice were divided into 3 groups: control, model, and GSK484 treatment groups. The model and GSK484 treatment groups were subjected to an AS model induction, followed by oral administration of 4 mg / kg GSK484 for a week in the treatment group, while the other groups received an equivalent volume of saline. Ankle joint damage scores, NETs levels, and the levels of PAD4, H3cit, IL-6, and IFN-γ were compared among the groups aftertreatment.
Results
Compared to healthy subjects, AS patients showed elevated levels of PAD4, H3cit,IL-1β, IL-6, and increased formation of NETs. The GSK484 treatment group exhibited reduced ankle joint damage scores, NETs formation, and levels of PAD4, H3cit, IL-1β, IL-6 compared to the modelgroup.
Conclusion
GSK484 inhibits the formation of NETs, offering a new therapeutic strategy for alleviating the inflammatory response in AS.
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Changes of LECT2 and FGF21 Levels in T2DM Patients Complicated with NAFLD and Their Clinical Significance
#br#
LU Junru, HOU Kaiwen, WANG Deying
Journal of Medical Molecular Biology 2024, 21 (
3
): 270-274. DOI: 10.3870/j.issn.1672-8009.2024.03.013
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Objective
To investigate the changes and clinical significance of serum leukocytederived chemotaxin 2 (LECT2) and fibroblast growth factor 21 (FGF-21) in patients with type 2diabetes mellitus (T2DM) complicated with non-alcoholic fatty liver disease ( NAFLD).
Methods
A total of 142 T2DM patients admitted to the
General Hospital of the Western Theater Region of the People
’
s Liberation Army of China
from October 2019 to October 2021 were divided into 2 groups according to whether complicated with NAFLD: with-NAFLD group (68 cases) and without-NAFLD group (74 cases). Clinical indicators of the patients were collected, and the levels of LECT2 and FGF-21 were detected by ELISA. The differences in clinical indicators between the two groups were compared, and the correlations between the levels of LECT2 and FGF-21 and the other clinical indicators were analyzed. Logistic regression analysis was used to analyze the independent influencing
factors of T2DM with NAFLD. ROC curve was used to analyze the efficacy of each variable in predicting T2DM with NAFLD.
Results
The values of BMI, WHR, SBP, DBP, FPG, FINS, FCP,HbAlc, HOMA-IR, TC, TG, LDL-C, ALT, AST, GGT, LECT2 and FGF21 in the withNAFLD group were higher than those in the without-NAFLD group, the values of HOMA-β andHDL-C were lower than those in the without-NAFLD group (
P
< 0. 05). Correlation analysis showedthat the level of LECT2 was positively correlated with the values of BMI, WHR, FPG, FINS, FCP, HbAlc, HOMA-IR, TC, GGT, and was negatively correlated with the values of HOMA-βand HDL-C (
P
<0. 05). The level of FGF21 was positively correlated with the values of FPG, FINS,FCP, HbAlc, HOMA-IR, TC and TG, but negatively correlated with the values of HOMA-β andHDL-C (
P
<0. 05). Logistic analysis showed that HOMA-IR, HDL-C, LECT2 and FGF21 were independent influencing factors of T2DM with NAFLD (
P
<0. 05). ROC curve analysis showed that theoptimal truncation values of LECT2 and FGF21 for predicting T2DM with NAFLD were 30. 72 ng / mL and 138. 66 ng / L, with 72. 61 % and 71. 36 % sensitivity and 72. 54 % and 73. 75 % specificity, respectively. The AUC values for LECT2 and FGF21 were 0. 732 and 0. 753, respectively. And the combined sensitivity, specificity and AUC values were 85. 72 % , 87. 44 % and 0. 863, respectively(
P
<0. 001).
Conclusion
LECT2 and FGF-21 are correlated with insulin resistance indicators andlipid levels, which can be used as indicators to predict T2DM with NAFLD.
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Canagliflozin Alleviates Renal Fibrosis in Diabetic Nephropathy Mice by PDGF / SIRT1
#br#
ZENG Weixin, YUN Chuan, LI Xiaoyan, LI Dawei
Journal of Medical Molecular Biology 2024, 21 (
3
): 275-279. DOI: 10.3870/j.issn.1672-8009.2024.03.014
Abstract
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20
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Objective
To investigate the potential mechanism of canagliflozin alleviating renal fibrosis in diabetic nephropathy mice through PDGF / SIRT1.
Methods
The diabetic nephropathymouse model was established using streptozotocin ( STZ), and the following groups were set up:① control mice, ② STZ mice, ③ STZ mice treated with canagliflozin, ④ BSA treated STZ mice,⑤ STZ treated with PDGF antibody, ⑥ STZ mice co-treated with canagliflozin and BSA, ⑦ STZmice co-treated with canagliflozin and PDGF antibody. The kidney tissues and serum of mice in eachgroup were collected. The mRNA and protein expression levels of myofibroblast markers (type I collagen, fibronectin, α-SMA ) were detected. The mitochondrial biogenesis indicators ( the mitochondrial DNA copy number and the expression levels of key regulatory factors SIRT1 and differentsubunits of electron transport chain proteins) were analyzed. And the levels of serum PDGF weremeasured.
Results
STZ significantly enhanced the mRNA and protein expression levels of type Icollagen, fibronectin and α-SMA. However, the expression levels of these myofibroblast markerswere returned to normal levels after canagliflozin treatment. STZ reduced mitochondrial DNA copynumber, and canagliflozin prevented this decline. At the same time, STZ-induced reductions in
SIRT1, PHB1, HSP60, VDHC, SDHA, and Cox IV were blocked by canagliflozin. Furthermore, the STZ-induced rise in PDGF level was restored by the presence of canagliflozin. The expression level of SIRT1 in the kidneys of STZ and PDGF co-treated mice was lower and the mRNA expression levels of myofibroblast markers were higher, when compared with those in the kidneys of of STZtreated mice. And there were no significant differences in the expression levels of SIRT1 and mRNA expression levels of myofibroblast markers in the kidneys of mice co-treated with STZ, PDGF and canagliflozin, when compared with those of the STZ mice co-treated with canagliflozin andBSA.
Conclusion
Canagliflozin therapy can reduce renal fibrosis in diabetic nephropathy mice andthe mechanism is dependent on the PDGF / SIRT1-mediated mitochondrial biogenesis axis.
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LINC
01138 Regulates Proliferation
,
Migration
,
and Invasion of SW620 Colorectal Cancer Cells through Targeting
miR-
559
#br#
GAO Dongyun, SUN Ting, CHEN Ping, ZHOU Xuefeng
Journal of Medical Molecular Biology 2024, 21 (
3
): 280-286. DOI: 10.3870/j.issn.1672-8009.2024.03.015
Abstract
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35
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Objective
To investigate the effect of
LINC
01138 on the proliferation, migration, and invasion of SW620 colorectal cancer cells and its mechanism.
Methods
RT-qPCR was used to detect the expression levels of
LINC
01138 and
miR-
559 in the human normal colonic mucosal cells (FHC) and the colorectal cancer cells (SW620). SW620 cells cultured
in vitro
were randomly divided into 6 groups: si-NC, si-
LINC
01138, si-
LINC
01138 + si-
miR-
559, mimic NC,
miR-
559 mimic and
LINC
01138 mimic +
miR-
559 mimic. CCK-8 assay, wound-healing assay, and transwellassay were performed to evaluate cell proliferation, migration, and invasion, respectively. The interaction between
LINC
01138 and
miR-
559 was validated using a dual-luciferase reporter assay.
Results
The expression level of
LINC
01138 was upregulated, while the expression level of
miR-
559 was downregulated in the SW620 cells when compared to those in the FHC. Inhibition of
LINC
01138 or upregulation of
miR-
559 attenuated the proliferation, migration, and invasion abilities of SW620 cells.
Conclusion
This study confirms the interaction between
LINC
01138 and
miR-
559 in colorectal cancer cells and reveals that
LINC
01138 regulates the proliferation, migration,and invasion of colorectal cancer cells through targeting
miR-
559. These findings provide new targetsand strategies for the treatment of colorectal cancer.
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Research Progress on
Aspergillus fumigatus
Associated C-type Lectin Receptor
#br#
CHENG He, MIAO Guizhi, MA Yan
Journal of Medical Molecular Biology 2024, 21 (
3
): 287-292. DOI: 10.3870/j.issn.1672-8009.2024.03.016
Abstract
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42
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Aspergillus fumigatus
(
A
.
fumigatus
) is the most prevalent airborne fungal pathogenand can cause fatal invasive aspergillosis in immunocompromised patients. The interaction of the pathogen with the host immune system is a key process in understanding pathogenicity. Recognition of conserved molecular structures on the surface of pathogens by conserved transmembrane or soluble pattern recognition receptors ( PRRs ) is referred to as pathogen-associated molecular patterns (PAMPs). C-type lectin receptors ( CLRs) are one of the major receptor families in PRRs, and CLRs can recognize fungal cell wall components such as β-glucan, mannose, and chitin through Ctype lectin-like domains ( CTLDs), thus inducing both innate and acquired immunity to clearpathogens. Currently, the main CLRs involved in
A
.
fumigatus
are Dectin-1, Dectin-2, MelLec, DC-SIGN, etc. These CLRs play a crucial role in host cell recognition of
A
.
fumigatus
, and novelanti-fumigatus drugs have been developed against Dectin-1 and Dectin-2. Therefore, further understanding of the effect of various CLRs associated with
A
.
fumigatus
and its mechanism and the relatedsignaling pathways will provide us new perceptions for the development of novel antifungal drugs. Inthis case, this paper presents a review of the latest research progress of CLRs related to
Aspergillus fumigatus
.
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GATA3 Inhibits Migration of Human Breast Cancer Cells by Regulating LIFR
#br#
ZHANG Lu, ZHANG Rui, LIU Jun, YANG Angang
Journal of Medical Molecular Biology 2024, 21 (
4
): 293-299. DOI: 10.3870/j.issn.1672-8009.2024.04.001
Abstract
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13
)
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Objective
To explore the effect of GATA binding protein 3 on the migration abilityof breast cancer cells.
Methods
Lentivirus-mediated GATA3-knockdown cell line was establishedto study the expression levels and function of GATA3 by performing real-time quantitative fluorescentPCR, Western blotting and Transwell assay
in vitro
. The binding sites of GATA3 in LIFR promoterregion was detected by Chromatin immunoprecipitation assay ( ChIP-qPCR) assay in MCF7 andT47D cells. LIFR was overexpressed in MCF7 cells with reduced GATA3 expression, and the migration capacity of MCF7 cells was measured by Wound healing assay and Transwell assay.
Results
Compared with the control group, the group of MCF7 cells that knocked down GATA3 had enhancedmigration ability (all
P
< 0. 05), and decreased expression of LIFR ( all
P
< 0. 05). ChIP-qPCRdata showed a physical binding of GATA3 on the promoter region of LIFR in MCF7 and T47D cells(all
P
< 0. 05). Overexpression of LIFR rescued the enhanced cell migration induced by depletion of GATA3 in MCF7 cells (all
P
< 0. 05).
Conclusion
GATA3 inhibits the migration of breast cancercells MCF7 through transcriptional activation of LIFR.
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Effect of miR-155 Target Gene
CEBPβ
on Apoptosis and Inflammatory Response of Intervertebral Disc Chondrocytes in Rat with Cervical Spondylosis through Regulation of NF-κB Signaling Pathway
#br#
NA Qing, Tuersunayi Abudureyimu, WU Gang
Journal of Medical Molecular Biology 2024, 21 (
4
): 300-308. DOI: 10.3870/j.issn.1672-8009.2024.04.002
Abstract
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9
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Objective
To explore the role and potential mechanisms of CCAAT-enhancerbinding protein β (C / EBPβtargeted by microRNA (miR) -155 in apoptosis and inflammatory response of rat intervertebral disc chondrocytes with cervical spondylosis.
Methods
Forty adult maleSD rats were randomly divided into 4 groups with 10 rats in each group: Sham group, CervicalSpondylosis group, Cervical Spondylosis + C / EBPβ overexpression group, and Cervical Spondylosis
+ empty vector group. Rat chondrocyte cell line, atdc5 cells, were divided into 6 groups: control group, tumor necrosis factor α ( TNF-α) stimulation group, empty vector + TNF-α group, C / EBPβ overexpression + TNF-α group, mimic-NC + C / EBPβ overexpression + TNF-α group, and miR-155 mimic + C / EBPβ overexpression + TNF-α group. The expression of miR-155, apoptosis-related proteins (cleaved-caspase3, Bax, Bcl-2, PPARγ), NF-κB signaling pathway proteins (pNF-κB P65, NF-κB P65, IκB), pro-inflammatory cytokines ( TNF-α, IL-6, IL-1β), and C / EBPβ in rat cartilage tissues and atdc5 cells were detected using qRT-PCR and Western blotting experiments. Dual-luciferase reporter gene assay was conducted to determine the targeted regulatoryeffect of miR-155 on C / EBPβ expression.
Results
miR-155, cleaved-caspase3, Bax, PPARγ,p-NF-κB P65, TNF-α, IL-6, and IL-1β were upregulated in the Cervical Spondylosis group when compared with those in the Sham group, while Bcl-2, IκB, and C / EBPβ were downregulated inthe Cervical Spondylosis group (
P
< 0. 05)Ceaved-caspase3, Bax, PPARγ, p-NF-κB P65, TNF-α, IL-6, and IL-1β were downregulated in the Cervical Spondylosis + C / EBPβ overexpression group when compared with those in the Cervical Spondylosis + empty vector group, while Bcl-2, IκB, and C / EBPβ were upregulated in the Cervical Spondylosis + C / EBPβ overexpression group(
P
< 0. 05), but there were no significant change in miR-155 expression level (
P
> 0. 05). There was a significant negative correlation between the expression levels of miR-155 and C / EBPβ in thecartilage of rats with cervical spondylosis (
r
= - 0. 721,
P
< 0. 05). The TNF-α group showed upregulations of miR-155, cleaved-caspase3, Bax, PPARγ, p-NF-κB P65, IL-6, and IL-1β expression (
P
< 0. 05), and downregulations of Bcl-2, IκB, and C / EBPβ expression when compared with the control group (
P
< 0. 05). The C / EBPβ overexpression + TNF-α group showed downregulations of cleaved-caspase3, Bax, PPARγ, p-NF-κB P65, IL-6, and IL-1β expression, and upregulations of Bcl-2, IκB, and C / EBPβ expression when compared with the empty vector + TNF-α group (
P
< 0. 05), but no significant change was observed in miR-155 expression level (
P
>0. 05). The mimic + C / EBPβ overexpression + TNF-α group showed upregulations of miR-155,cleaved-caspase3, Bax, PPARγ, p-NF-κB P65, IL-6, and IL-1β expression (
P
< 0. 05), anddownregulations of Bcl-2, IκB, and C / EBPβ expression when compared with the mimic-NC + C /EBPβ overexpression + TNF-α group (
P
< 0. 05). Dual-luciferase reporter gene assay confirmed
CEBPβ
as a target gene of miR-155 in chondrocytes.
Conclusion
miR-155 promotes the activationof the NF-κB signaling pathway in intervertebral disc cartilage tissues and chondrocytes in rat withcervical spondylosis by inhibiting the target gene
CEBPβ
, which leads to enhanced apoptosis and inflammatory response.
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Effect of Extracellular Histone on Epithelial Mesenchymal Transformation and Invasion of Bladder Cancer Cells by Regulation of TLR4 / NF-κB Pathway
#br#
HAN Zhijun, SHU Linfei, YI Xiangmeng, TAN Huajun, ZHENG Guoqiu, YANG Fan
Journal of Medical Molecular Biology 2024, 21 (
4
): 309-314. DOI: 10.3870/j.issn.1672-8009.2024.04.003
Abstract
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10
)
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Objective
To investigate the effect of extracellular histone on epithelial mesenchymal transformation (EMT) and invasion of bladder cancer cells by regulating toll-like receptor 4(TLR4) / nuclear factor-κB (NF-κB) pathway.
Methods
T24 bladder cancer cells were culturedand divided into 7 groups: control group, histone H3 groups with different concentrations (50, 100, 200 μg / mL), solvent control (0. 1 % DMSO) group, histone H3 (200 μg / mL) + solvent control (0. 1 % DMSO) group, and histone H3 (200 μg / mL) + NF-κB inhibitor Bay11-7082 (10 μmol / L) group. The number of invasion cells and the protein expression levels of E-cadherin, N-cadherin, Vimentin, TLR4 and phosphorylated P65 NF-κB ( p-P65 NF-κB) were detected 24 h after administration.
Results
The number of invasion cells and the expression levels ofN-cadherin, Vimentin, TLR4 and p-P65 NF-κB in the histone H3 groups were higher than those inthe control group, and the protein expression level of E-cadherin was lower than that in the controlgroup (
P
< 0. 05), the number of invasion cells and the expression levels of those proteins werechanged with the concentration of histone H3 treatment in a dose-dependent manner. The number ofcell invasion and the protein expression levels of N-cadherin, Vimentin and p-P65 NF-κB in thehistone H3 + Bay11-7082 group were lower than those in the histone H3 + solvent control group,
and the expression level of E-cadherin was higher than that in the histone H3 + solvent control group(
P
< 0. 05).
Conclusion
Extracellular histone promotes EMT and invasion of bladder cancer cells,which is related to the activation of TLR4 / NF-κB pathway.
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Effect of TLR2-mediated Microglia Activation and Neuroinflammation on Vascular Dementia Progression
#br#
SUN Yangzi, WU Zhenyu, ZENG Chaosheng, YOU Yong
Journal of Medical Molecular Biology 2024, 21 (
4
): 315-322. DOI: 10.3870/j.issn.1672-8009.2024.04.004
Abstract
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15
)
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Objective
To investigate the effect of TLR2 in mediating the pathological activation of microglia and neuronal injury in vascular dementia ( VaD) rat model and its molecularmechanisms.
Methods
In vitro
experiments were carried out by using LPS-induced activation of human microglia cell line HMC3 cells. The proliferation ability of HMC3 cells was determined by CCK- 8 assay. Systemic TLR2 knockdown was performed by using Adv-TLR2 shRNA or Adv-shRNA NT. The VaD rat model was established by permanent bilateral common carotid artery occlusion (2VO) . The expression levels of TLR2, NF-κB, Iba-1, Claudin-5 and ZO-1 in HMC3 cells and rats’white matter tissues were determined by Western blotting. The levels of inflammatory cytokines IL-6, IL-1β and TNF-α, and the ferroptosis-related indicators of Fe
2 +
, malondialdehyde (MDA) and glutathione (GSH) in rats’white matter tissues were determined by ELISA. Morris water maze
(MWM) test was used to determine rats’brain neuronal injury.
Results
The expression levels ofTLR2, NF-κB and Iba-1 in the LPS group were enhanced when compared with those in the Controlgroup (
P
< 0. 05). The expression levels of the above proteins in the Adv-TLR2 shRNA group were decreases when compared with those in the LPS groups (
P
< 0. 05). The expression levels ofTLR2 / NF-κB and Iba-1 were up-regulated, and those of Claudin-5 and ZO-1 were down-regulatedin the white matter tissues of Model group rats, when compared with those of the Sham group, (
P
<0. 05). In addition, the levels of inflammatory cytokines IL-6, IL-1β and TNF-α were up-regulated(
P
< 0. 05), the Fe
2 +
and MDA levels were increased, and the GSH levels were decreased (
P
<0. 05). TLR2 knockdown had reversed the values of above indicators in the Model + Adv-TLR2 shRNA group when compared with those in the Model group (
P
< 0. 05). Morris water maze test showedthat rats in the Model group and Model + Adv-TLR2 shRNA group took longer time to find the targetquadrant (upper left quadrant) (
P
< 0. 05), stayed shorter time in the target quadrant (
P
<0. 05) when compared with those in the Sham group, the swimming routes of rats in the four quadrants of MWM were evenly distributed. Compared with Model group, the Model + Adv-TLR2 shRNAgroup showed a reversion in the values of above indicators and had a denser distribution of swimroutes in the target quadrant.
Conclusion
Knock-down of TLR2 could inhibit the activation of microglia and its mediated tight junction protein degradation and cerebrovascular barrier network leakage, and reduce nerve damage in the vascular dementia rat model.
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Effect of Knocking down Astrocyte Elevated Gene-1 on Diethylnitrosamine-induced Primary Hepatocellular Carcinoma in Rats
#br#
CHEN Jianxiong, JI Ru, CAI Qing, ZHANG Qian
Journal of Medical Molecular Biology 2024, 21 (
4
): 323-328. DOI: 10.3870/j.issn.1672-8009.2024.04.005
Abstract
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22
)
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Objective
To explore the effect of knocking down astrocyte elevated gene-1 (
AEG-
1 ) on diethylnitrosamine ( DEN ) -induced primary hepatocellular carcinoma ( PHC ).
Methods
A total of 60 rats were randomly divided into 4 groups: Control group, DEN group,AEG-1 NC KO DEN group and AEG-1 KO DEN group, 15 rats in each group. Rats were given intragastric administration of DEN to construct PHC models in each group except in the Control group, while rats in the Control group were given the same volume of normal saline. The rats in AEG-1 KO DEN group and AEG-1 NC KO DEN group were given intraperitoneal injection of HCCLM6 withstably transfected
AEG-
1 shRNA or shRNA-NC lentivirus expression vector, respectively. The liver cell damage, apoptosis, levels of superoxide dismutase ( SOD), malondialdehyde ( MDA) and glutathione peroxidase (GSH), liver function, levels of serum IL-6 and TNF-α, expressions of caspase-3 (Cas-3), caspase-9 ( Cas-9 ) and P65 in liver tissues were compared among eachgroup.
Results
The expression level of
AEG-
1 in the DEN group was significantly higher than that in the Control group (
P
< 0. 05). The mortality of rats and incidence of ascites in the AEG-1 KO DEN group were lower than those in the DEN group (
P
< 0. 05), and the levels of serum AST,
ALT, IL-6 and TNF-α were lower than those in the DEN group (
P
< 0. 05), SOD activity was higher than that in the DEN group (
P
< 0. 05), levels of GSH and MDA were lower than those in the DEN group (
P
< 0. 05), and expressions levels of cleaved cas9 / cas9, cleaved cas3 / cas3 and p-P65 / P65 were lower than those in the DEN group (
P
< 0. 05).
Conclusion
Knocking out
AEG-
1can reduce the levels of oxidative stress and inflammatory factors induced by DEN, relieve liver tissue damage and improve liver function in rats.
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Effect of MRPL21 on Activity of Non-small Cell Lung Cancer A549 Cells by Regulating YAP1 / TAZ Pathway
#br#
FANG Hanlin, PAN Huaguang, CHEN Yu, ZHANG Renquan
Journal of Medical Molecular Biology 2024, 21 (
4
): 329-333. DOI: 10.3870/j.issn.1672-8009.2024.04.006
Abstract
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10
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Objective
To investigate the effect of MRPL21 and YAP1 / TAZ pathway on theactivity of non-small cell lung cancer A549 cells, so as to provide new ideas for the treatment ofnon-small cell lung cancer.
Methods
Non-small cell lung cancer tissues and adjacent tissues were obtained from 9 patients with non-small cell lung cancer who underwent surgical treatment in
the First Affiliated Hospital of Anhui Medical University
between June, 2021 and September, 2023. Theexpression of MRPL21 in the tissues was analyzed by immunohistochemistry. A549 cells were randomly divided into three groups: siNC group, siMRPL21 group and BPD-MA group. CCK-8 assay and Hoechst staining were used to detect the proliferation of A549 cells. Transwell assay was used to analyze the invasion ability of A549 cells. TUNEL staining was used to detect the apoptosis of A549 cells. Western blotting assay was used to detect the expression levels of MRPL21, YAP1 and TAZproteins in A549 cells.
Results
The results of immunohistochemistry showed that the expression ofMRPL21 was up-regulated in the non-small cell lung cancer tissues compared with that in the adjacent tissues (
P
< 0. 05). Compared with the A549 cells in the siNC group, cells in the siMRPL21group and the BPD-MA group showed decreased proliferation ability as detected by CCK8 assay and
Hoechst staining assay (
P
< 0. 05). Transwell assay showed that the invasion abilities of A549 cells in the siMRPL21 group and the BPD-MA group were decreased (
P
< 0. 05 ). TUNEL stainingshowed that the apoptosis rates of A549 cells were increased in the siMRPL21 group and the BPDMA group (
P
< 0. 05). Western blotting results showed that the siMRPL21 group and the BPD-MA group had significant reduced protein levels of YAP1 and TAZ in A549 cells (
P
< 0. 05).
Conclusion
MRPL21 is highly expressed in non-small cell lung cancer tissues. After inhibiting the expression of MRPL21, the proliferation activity and invasion ability of A549 cells are weakened, and the apoptosis rate is increased, which is related to the regulation of YAP1 / TAZ signaling pathway. MRPL21 is expected to be a new target for the treatment of non-small cell lung cancer.
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Effect of miR-424 on Proliferation and Apoptosis of Multiple Myeloma Cells by Targeting
FBXW
7
#br#
DUAN Xiaojuan, XI Zhenfang, HOU Ruihong
Journal of Medical Molecular Biology 2024, 21 (
4
): 334-340. DOI: 10.3870/j.issn.1672-8009.2024.04.007
Abstract
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11
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Objective
To investigate the effect of miR-424 on the proliferation and apoptosisof multiple myeloma ( MM) cells by targeting the F-box and WD repeat domain containing 7(
FBXW
7).
Methods
Real-time fluorescence quantitative PCR ( RT-qPCR) experiment was applied to detect the expression levels of miR-424 and
FBXW
7 in human normal bone marrow plasma cells and MM cell lines MM. 1S, RPMI 8226, U266. U266 cells were cultured
in vitro
and randomly separated into 5 groups: control group, miR-424 inhibitor group,
FBXW
7 overexpression group, negative control group, miR-424 inhibitor +
FBXW
7 knockdown group. Edu staining and TUNELstaining were applied to detect the cell proliferation and apoptosis, respectively. Western blotting assay was applied to detect the expression levels of proliferation related proteins ( Cyclin D1, PCNA), apoptosis related proteins (Bax, Bcl-2), and FBXW7 protein. A nude mouse model of multiple myeloma transplantation was constructed by subcutaneous inoculation of transfected U266 cells in the right axilla of nude mice, the growth of the transplanted tumors were detected and the transplanted tumor volume was compared on the 21st day. Dual luciferase reporter experiment was applied
to verify the targeted regulatory effect of miR-424 on
FBXW
7 in U266 cells.
Results
In comparisonwith those in the normal human bone marrow plasma cells, the expression of miR-424 in theMM. 1S, RPMI 8226, and U266 cells were increased (
P
< 0. 05 ), while the expression of
FBXW
7 mRNA were decreased (
P
< 0. 05). In addition, when compared with the control group, the miR-424 inhibitor group and the
FBXW
7 overexpression group showed decreased cell proliferation rate, lower protein expression levels of Cyclin D1, PCNA and Bcl-2, and decreased transplanted tumor volume on the 21st day (
P
< 0. 05), and increased apoptosis rate,
FBXW
7 mRNA and protein expression levels, and Bax protein expression level (
P
< 0. 05). There was no significant difference in the indicators in cells of the negative control group (
P
> 0. 05). Moreover, when compared with the miR-424 inhibitor group, the miR-424 inhibitor +
FBXW
7 knockdown group exhibited increased cell proliferation rate, Cyclin D1, PCNA and Bcl-2 protein expression, and transplanted tumor volume on the 21st day (
P
< 0. 05), and decreased apoptosis rate,
FBXW
7 mRNA and protein expression levels, and Bax protein expression level (
P
< 0. 05). It was also observed that miR-424 was able to targetly downregulate
FBXW
7 expression in U266 cells.
Conclusion
Down-regulation of miR-424 can inhibit MM cell proliferation and growth in nude mice, and promote the apoptosis by up-regulating
FBXW
7 expression.
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Nerve Growth Factor Combined with BMSCs Exosomes Alleviates Neural Injury in Rats with Intracerebral Haemorrhage through Keap1 / NQO1 / Nrf2 Signaling Pathway
#br#
LI Fang, TANG Shijun, Maimaitiyiming Tuoheti
Journal of Medical Molecular Biology 2024, 21 (
4
): 341-346. DOI: 10.3870/j.issn.1672-8009.2024.04.008
Abstract
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7
)
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Objective
To explore the therapeutic effect and mechanisms of rat nerve growthfactor (RtNGF) combined with bone marrow mesenchymal stem cell-derived exosomes ( BMSCs exosomes) on neural injury of intracerebral haemorrhage (ICH) rats.
Methods
The BMSCs exosomes were prepared for the following experiments. Sixty rats were randomly divided into 5 groups: Sham group, ICH group, ICH + RtNGF group, ICH + BMSCs exosomes group, and ICH + RtNGF + BMSCs exosomes group, with 12 rats in each group. A ICH rat model was established and RtNGF or BMSCs exosomes were treated alone or in combination. Paraffin embedded tissue sections of rat brain tissues in each group were prepared and HE staining was performed. qPCR and Immunohistochemistry were used to determine the mRNA and protein expression levels of genes in the Keap1 / NQO1 /Nrf2 signaling pathway.
Results
Significant existence of tissue lacunes and blood clots were observed in the ICH group rather than in the Sham group. RtNGF or / and BMSCs treatments improved that situation, and the combination of RtNGF and BMSCs exosomes treatment had the best effect on
alleviating neural injury. The mRNA expression levels of Keap1, NQO1 and Nrf2 in the brain tissues, and the IHC relative staining scores of the three proteins in the ICH group were increasedwhen compared with those in the Sham group ( all
P
< 0. 05). The levels of the above indicators inthe ICH + RtNGF group, ICH + BMSCs exosomes group, and ICH + RtNGF + BMSCs exosomesgroup were decreased when compared with those in the ICH group (
P
< 0. 05), with the values the lowest in the ICH + RtNGF + BMSCs exosomes group (
P
< 0. 05).
Conclusion
RtNGF combinedwith BMSCs exosomes has significant effect on reducing oxidative stress and alleviating neural injury through Keap1 / NQO1 / Nrf2 signaling pathway in ICH rats.
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hsa
_
circRNA
_ 002178 Gene Interference Inhibits Malignant Biological Behavior of Ovarian Cancer Cells
#br#
PENG Hu, LONG Chenglan, LUO Ting, YIN Bangchao, ZHOU Jian
Journal of Medical Molecular Biology 2024, 21 (
4
): 347-353. DOI: 10.3870/j.issn.1672-8009.2024.04.009
Abstract
(
7
)
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2
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Objective
To study the effect of
circRNA
_ 002178 gene interference on malignant biological behavior of ovarian cancer cells.
Methods
Human ovarian cancer SKOV3 cells were divided into 4 groups: control group, short hairpin RNA negative control (shRNA-NC) group, circRNA_ 002178-shRNA 1 group and circRNA_ 002178-shRNA 2 group. The expression level of circRNA_ 002178 was detected by real-time fluorescence quantitative polymerase chain reaction (RTPCR). Flow cytometry was used to detect the cell apoptosis and mitochondrial membrane potential and to select the stem cell positive (CD44, CD133) cell lines. The stem cell spheroidization test was used to detect the sphere formation rate and the diameter of spheres. Transwell assay was used to detect the cell invasion. Western blotting was used to detect the expression levels of the proteins. Thetransplanted tumor model was constructed to observe the effect of
circRNA
_ 002178 gene interference on tumor formation.
Results
CircRNA_ 002178 interference significantly promoted the apoptosis ofSKOV3 cells, decreased the number of CD44 and CD133 positive cells, the rate of sphere formation, the diameter of spheres and the number of invasive cells, intensified the changes of mitochon
drial membrane potential, and inhibited tumor growth and Akt / mTOR pathway activation in transplanted tumor rats.
Conclusion
CircRNA_ 002178 interference can inhibit the malignant biologicalbehavior of ovarian cancer cells. The mechanism may be related to the inhibitory effect on Akt / mTOR pathway.
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Anti-Tumor Effect of Kaempferol on Esophageal Squamous Cell Carcinoma through PI3K / AKT Signaling Pathway
#br#
YANG Zhao, ZANG Ting , MA Kai , WANG Zhuangzhuang , LI Wenhai , ZHOU Jincai
Journal of Medical Molecular Biology 2024, 21 (
4
): 354-360. DOI: 10.3870/j.issn.1672-8009.2024.04.010
Abstract
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8
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Objective
To investigate the anti-tumor effect and potential mechanism ofkaempferol on esophageal squamous cell carcinoma (ESCC) cells.
Methods
CCK-8, colony formation and flow cytometry were used to determine the effect of kaempferol on the proliferation andapoptosis of ECA-109 cells. Transwell assay was used to detect cell invasion. Western blotting wasemployed to measure the protein expression levels.
Results
Compared with the 0 μmol / L kaempferol group, the 40 μmol / L and 60 μmol / L kaempferol groups had significantly inhibited proliferationand invasion of ECA-109 cells and enhanced apoptosis. Moreover, kaempferol (40 μmol / L and 60μmol / L ) had significantly decreased expression levels of proliferating cell nuclear antigen (PCNA) and Ki67, and lower phosphorylation levels of phosphatidylin-ositol-3-kinase ( PI3K) and protein kinase B ( AKT), and increased expression levels of pro-apoptosis-related proteins. In addition, PI3K activator 740Y-P reversed the regulatory effect of kaempferol on proliferation, invasion and apoptosis of ECA-109 cells.
Conclusion
Kaempferol inhibits the proliferation, invasion and inducesthe apoptosis of ECA-109 cells by inhibiting PI3K / AKT signaling pathway.
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Expression of MyD88 / IL-23 and Liver Regeneration after Hepatectomy in Mice with Subcutaneous Infection of
E
.
granulosus
#br#
CHEN Jun, YU Peng
Journal of Medical Molecular Biology 2024, 21 (
4
): 361-365. DOI: 10.3870/j.issn.1672-8009.2024.04.011
Abstract
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13
)
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1
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Objective
To explore the influence of
Echinococcus granulosus
, (
E
.
granulosus
)infection on liver regeneration in hepatectomy model in mice, and to investigate the expression ofMyD88 / IL-23 in the liver regeneration of
E
.
granulosus
-infected mice post hepatectomy and its significance.
Methods
A mouse model with 70 % hepatectomy following subcutaneous infection of
E
- .
granulosus
was established. A total of 18
E
.
granulosus
-infected mice and 18 healthy mice as controls were chosen for the surgery. The amount and rate of liver regeneration at different time points post-surgery in mice between the two groups were analyzed. The expression levels of MyD88 and IL-23 in mouse serum at different time points were measured by ELISA. The changes in hepatic functionindicators AST and ALT were also monitored.
Results
Compared to the control mice, the
E
-.
granulosus
-infected mice demonstrated decreased liver regeneration amount and regeneration ratepost hepatectomy, with significant differences apparent at the time points of 12 hours, 1 day, and2 days post-surgery. In comparison to the control mice, the
E
.
granulosus
-infected mice exhibitedmarkedly increased levels of AST and ALT in peripheral blood 1 day post-surgery, and notably increased levels of MyD88 and IL-23 2 hours post-surgery.
Conclusions
E
.
granulosus
infection significantly decelerates the liver regeneration process following hepatectomy in mice, which maythrough increasing the levels of MyD88 and IL-23.
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Bioinformatics Analysis of circRNA-miRNA-mRNA ceRNA Network for Prognosis in Gastric Cancer
#br#
HUANG Xinyi, ZHOU Jintao, JIANG Chenshan
Journal of Medical Molecular Biology 2024, 21 (
4
): 366-373. DOI: 10.3870/j.issn.1672-8009.2024.04.012
Abstract
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10
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Objective
To construct a prognostic circRNA-miRNA-mRNA ceRNA network ingastric cancer ( GC) and explore the diagnostic and therapeutic targets.
Methods
Differentiallyexpressed circular RNAs (circRNA), related microRNAs (miRNA) and mRNAs in GC were obtained from GEO and TCGA databases. Cytoscape was utilized to construct the circRNA-miRNA-mRNA ceRNA network, to understand the biological functions of differentially expressed mRNAs and identifying the hub genes. Kaplan-Meier survival analysis was used to verify the prognostic values.
Results
The ceRNA network was consisted of 2 circRNAs, 5 miRNAs and 349 mRNAs thatwere differentially expressed. Functional enrichment analysis revealed that mRNAs were significantly enriched in terms and pathways like “ muscle system process”, “ metal ion transmembrane transporter activity”, “synaptic membrane” and “calcium signaling pathway” . A PPI network containing 125 nodes and 165 edges was constructed and 10 hub genes were identified. Survival analysis implied that low ADAR1D or PTGFR expression levels might lead to poor prognosis of GC patients.
Conclusion
The circRNA-miRNA-mRNA ceRNA network involved in prognosis of GC issuccessfully constructed. Two axes, the hsa _ circ _ 0001190 / hsa-miR-7-5p / ADRA1D and the hsa_ circ_ 0036287 / hsa-miR-3127-5p / PTGFR, are identified with potential prognostic values in GC, providing a new target for diagnosis andtreatment of GC.
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Bioinformatics Analysis of Common Key Genes and Signal Pathways in Liver Cancer and Diabetes
#br#
ZHOU Yilin, JI Haitao, WANG Yanfeng
Journal of Medical Molecular Biology 2024, 21 (
4
): 374-379. DOI: 10.3870/j.issn.1672-8009.2024.04.013
Abstract
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10
)
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Objective
To explore the gene features and pathogenic mechanisms shared byhepatocellular carcinoma and diabetes mellitus using bioinformatics methods.
Methods
The hepatocellular carcinoma dataset (GSE121248) and diabetes mellitus dataset ( GSE29221) were downloaded from the GEO (Gene Expression Omnibus) database, and were analyzed by R. Venn diagrams were used to obtain the shared differentially expressed genes (DEGs). GO (gene ontology) and KEGG ( kyoto encyclopedia of genes and genomes) enrichment analyses were performed on DEGs, and Cytoscape software was used to obtain the key modules and core genes in the proteinprotein interaction (PPI) network. The network interaction analyses of genes, transcription factors and mi-RNAs were performed in NetworkAnalyst database. DGIdb database was used for gene-drug interaction analysis. The prognostic values of the core genes were analyzed by Kaplan-Meier Plotterdatabase.
Results
A total of 39 DEGs were screened out, which were significantly enriched inpathways such as extracellular matrix, positive regulation of insulin-like growth factor receptor signaling pathway, heparin binding, and P53 signaling pathway. 6 core genes (
THBS
1,
DCN
,
BGN
,
COL
14
A
1,
LUM
and
PCOLC
) were screened out, of which two core genes (
DCN
and
THBS
1) could interacted with some tumor therapeutic agents and one core gene (
DCN
) was associat
ed with the prognosis of hepatocellular carcinoma patients.
Conclusion
DCN
may be a potentialdrug therapeutic target for patients with both diabetes and hepatocellular carcinoma.
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Relationship between Serum Hcy
,
CysC
,
D-D Levels and Condition of Patients with Acute Ischemic Stroke and Their Short-term Prognosis after Intravenous Thrombolysis
#br#
WANG Wenjing, LI Lina, WANG Jicun
Journal of Medical Molecular Biology 2024, 21 (
4
): 380-385. DOI: 10.3870/j.issn.1672-8009.2024.04.014
Abstract
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10
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Objective
To investigate the relationship between serum homocysteine ( Hcy),cystatin C (CysC) and D-dimer ( D-D) levels and the condition and short-term prognosis of patients with acute ischemic stroke ( AIS) after intravenous thrombolysis.
Methods
A total of 100AIS patients who received intravenous thrombolytic therapy in
Shunyi District Hospital
from October2019 to June 2023 were selected. According to the National Institutes of Health Stroke Scale (NIHSS) score, the patients were divided into 3 groups: mild defect group (1-4 points, 44 cases),
moderate defect group (5-15 points, 29 cases) and severe defect group (16-42 points, 27 cases). According to the volume of cerebral infarction, the patients were divided into 3 groups: small infarction group ( < 5 cm
3
, 40 cases), moderate infarction group (5 ~ 15 cm
3
, 37 cases), and large infarction group ( > 15 cm
3
, 23 cases). Three months after intravenous thrombolysis, the patients were divided into 2 groups: good prognosis group (≤2 points, 75 cases) and poor prognosis group ( > 2 points, 25 cases), according to the modified Rankin scale score. Baseline data of patients were collected, and serum Hcy, CysC and D-D levels were detected. The changes of serum Hcy, CysC and D-D levels in AIS patients with different degrees of neurological deficit, cerebral infarction volume and short-term prognosis were compared. Pearson correlation coefficient was used to analyze the correlation between serum Hcy, CysC and D-D levels and AIS condition. Multivariate logistic regression was used to analyze the independent influencing factors of short-term prognosis of AIS. The receiver operating characteristic (ROC) curve was used to evaluate the predictive value of serum Hcy, CysC and D-D levels for short-term prognosis after AIS intravenous thrombolysis.
Results
The levels of serum Hcy, CysC and D-D in the mild defect group were the lowest, followed by the moderate defect group, and the severe defect group was the highest, with statisticallysignificant (
P
< 0. 05). The levels of serum Hcy, CysC and D-D in the small infarction group werethe lowest, followed by the moderate infarction group, and the large infarction group was the highest, the difference between the groups was statistically significant (
P
< 0. 05). Pearson correlationcoefficient analysis showed that serum Hcy, CysC and D-D levels were positively correlated withNHISS score (
r
= 0. 424, 0. 573, 0. 716, all
P
< 0. 001) and cerebral infarction volume (
r
=0. 633, 0. 479, 0. 548, all
P
< 0. 001). Univariate analysis showed that the levels of serum Hcy,CysC and D-D in the good prognosis group were lower than those in the poor prognosis group (all
P
< 0. 05). Multivariate logistic regression analysis showed that Hcy, CysC and D-D (OR = 1. 093,1. 343, 1. 146) were independent predictors of short-term prognosis of AIS (
P
< 0. 05). ROC curveanalysis showed that the area under the curve of serum Hcy, CysC, D-D and the combination of thethree in predicting the short-term prognosis of AIS was 0. 853, 0. 873, 0. 792 and 0. 946, respectively, and the combination of the three had the highest predictive value.
Conclusion
The levels ofserum Hcy, CysC and D-D are positively correlated with the severity of AIS patients, which can beused as predictors of short-term prognosis after intravenous thrombolysis in AIS patients.
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Progress in the Application of Lipidomics in Lung Cancer Research
#br#
LIANG Yi, YU Wanjun, LI Jiawei, XU Tao
Journal of Medical Molecular Biology 2024, 21 (
4
): 386-390. DOI: 10.3870/j.issn.1672-8009.2024.04.015
Abstract
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14
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In recent years, the application of lipidomics in lung cancer research has receivedincreasing attention, providing new perspectives on understanding the pathogenesis and therapeutic strategies of lung cancer. With technological advances, lipidomics will play a more critical role in lung cancer research and provide more specific biomarkers and pharmacodynamic evaluation tools for early diagnosis, condition monitoring, and personalized treatment of lung cancer. This review discusses the critical roles of core technologies like mass spectrometry and bioinformatics in lung cancer research. It also emphasizes the importance of serum and tissue-based lipidomics analysis in exploring specific biomarkers and differences between subtypes of lung cancer. Novel lipidomics strategies provide new directions for elucidating lung cancer pathogenesis and therapeutic strategy selection.
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