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).

Abstract

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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