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DNM3 Attenuates Hepatocellular Carcinoma Growth by Activating P53
Zhengdong Zhang1, Chun Chen2, Weike Guo3
1Department of General Surgery, The Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China (mainland).
Background:
Primary hepatocellular carcinoma is one of the most common malignant tumors in China and its mortality rate shows no sign at present of ceasing to rise. In our previous study, we found that the mRNA level of Dynamin3 (DNM3), a member of the Dynamin family, is significantly lower in hepatocellular carcinoma tissues than in non-tumor tissues. The aim of this study was to investigate the expression pattern and potential function of DNM3 in hepatocellular carcinoma.
Material/Methods:
First, we determined the expression ofDNM3 in human hepatocellular carcinoma tissues and cell lines. We then studied the biological function of DNM3 on hepatocellular carcinoma cells by proliferation assay and colony formation assay. Flow cytometry was used to study the effect of DNM3 on cell cycle and apoptosis.
Results:
Expression of DNM3 was significantly downregulated in hepatocellular carcinoma tissues and was associated with vein invasion and tumor metastasis. In addition, upregulation of DNM3 reduced hepatocellular carcinoma cell proliferation and colony formation, induced hepatocellular carcinoma cell G0/G1 phase arrest, and stimulated hepatocellular carcinoma cell apoptosis. We also found that DNM3 may exert its anti-proliferative effect through upregulating p53.
Conclusions:
Our findings suggest that DNM3 attenuates the proliferation and induces apoptosis of gastric cancer cells. Modulation of DNM3 may prove to be an efficient method of hepatocellular carcinoma treatment.
Insights
Dynamin3 (DNM3) is downregulated in hepatocellular carcinoma. Upregulating DNM3 inhibits cancer cell growth and promotes apoptosis, suggesting DNM3 as a potential therapeutic target for liver cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Hepatocellular carcinoma (HCC) is a prevalent malignancy in China with rising mortality.
- Previous studies indicated reduced Dynamin3 (DNM3) mRNA levels in HCC tissues.
- The role of DNM3 in HCC pathogenesis requires further investigation.
Purpose of the Study:
- To investigate the expression pattern of DNM3 in HCC.
- To elucidate the functional role of DNM3 in HCC progression.
- To explore the therapeutic potential of modulating DNM3 in HCC.
Main Methods:
- DNM3 expression analysis in HCC tissues and cell lines.
- In vitro functional assays: proliferation, colony formation, cell cycle, and apoptosis.
- Correlation analysis of DNM3 expression with clinical parameters.
Main Results:
- DNM3 expression is significantly downregulated in HCC tissues and correlates with vein invasion and metastasis.
- Overexpression of DNM3 suppresses HCC cell proliferation and colony formation.
- DNM3 upregulation induces G0/G1 cell cycle arrest and promotes apoptosis in HCC cells, potentially via p53 pathway activation.
Conclusions:
- DNM3 exhibits tumor-suppressive properties in HCC by inhibiting proliferation and inducing apoptosis.
- Modulating DNM3 expression presents a promising therapeutic strategy for HCC treatment.
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