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[Effects of hepatitis B virus X gene on p21(WAF1) expression through p53-dependent and p53-independent pathways]

Jing Lin1, Ming-Hua Zhu, Jian-Hui Qu

  • 1Department of Pathology, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, P.R.China.

AI Zheng = Aizheng = Chinese Journal of Cancer
|July 14, 2004
PubMed
Abstract

Insights

The hepatitis B virus X protein (HBx) impacts p53 and p21(WAF1) gene expression in liver cancer cells. HBx can inhibit p21(WAF1) promoter activity independently of p53, affecting cell cycle progression.

Area of Science:

  • Hepatology
  • Molecular Biology
  • Oncology

Background:

  • Hepatitis B virus X protein (HBx) is known to interfere with p53 tumor suppressor function.
  • The precise mechanism by which HBx influences p21(WAF1), a downstream target of p53, remains unclear.
  • This study investigates the effect of HBx on the p21(WAF1) gene in hepatoma cells.

Purpose of the Study:

  • To elucidate the mechanism of HBx's influence on p21(WAF1) gene expression.
  • To determine whether HBx affects p21(WAF1) transcription in a p53-dependent or independent manner.
  • To analyze the impact of HBx on hepatoma cell cycle progression.

Main Methods:

  • Co-transfection of wild-type p53 (wtp53) and HBx into SMMC-7721 cells.
  • Transfection of HBx alone into various hepatoma cell lines with differing endogenous p53 statuses.
  • Luciferase reporter assays to measure p21(WAF1) promoter activity.
  • Western blot analysis to assess p53 and p21(WAF1) protein expression.
  • Flow cytometry to evaluate cell cycle distribution.

Main Results:

  • HBx co-transfection with sense-wtp53 in SMMC-7721 cells increased luciferase activity compared to wtp53 alone.
  • HBx transfection generally decreased p21(WAF1) expression and promoter activity in hepatoma cells, particularly those with low p53.
  • Cell cycle analysis revealed altered G(0)/G(1) phase arrest in HBx-transfected cells, with variations depending on cell line and p53 status.

Conclusions:

  • HBx may enhance p21(WAF1) expression through cytoplasmic p53 accumulation.
  • HBx appears to inhibit p21(WAF1) promoter transcriptional activity via a p53-independent pathway.
  • These findings suggest a complex role for HBx in regulating cell cycle and gene expression in liver cancer.

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