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Hepatitis C virus E2 protein promotes human hepatoma cell proliferation through the MAPK/ERK signaling pathway via

Lan-Juan Zhao1, Lu Wang, Hao Ren

  • 1Department of Microbiology, Second Military Medical University, 800 Xiang-Yin Road, Shanghai 200433, China.

Experimental Cell Research
|March 22, 2005
PubMed

Insights

Hepatitis C virus E2 protein activates the MAPK/ERK pathway, promoting liver cell proliferation. This process is mediated by CD81 and LDLR cell receptors, highlighting a key mechanism in viral pathogenicity.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Signaling

Background:

  • Mitogen-activated protein kinase (MAPK) pathway dysregulation is linked to viral pathogenicity.
  • Hepatitis C virus (HCV) infection causes liver disease through abnormal intracellular signaling.
  • Transmembrane signal transduction by HCV E2 protein is not well understood.

Purpose of the Study:

  • To investigate the regulation of the MAPK/extracellular signal-regulated kinase (MAPK/ERK) pathway by HCV E2 protein.
  • To elucidate the role of cell surface receptors in E2-mediated signaling.
  • To understand how E2 influences target cell proliferation.

Main Methods:

  • Expression of HCV E2 protein in Chinese hamster oval cells.
  • Analysis of MAPK/ERK pathway activation in human hepatoma Huh-7 cells.
  • Investigation of CD81 and low-density lipoprotein receptor (LDLR) roles using blockage and inhibitors (U0126).

Main Results:

  • HCV E2 protein specifically activated the MAPK/ERK pathway and downstream ATF-2 transcription factor.
  • E2 significantly promoted Huh-7 cell proliferation.
  • CD81 and LDLR mediated E2 binding, and their blockage suppressed MAPK/ERK activation and proliferation.
  • MEK1/2 inhibitor U0126 also impaired E2-induced MAPK/ERK activation and cell proliferation.

Conclusions:

  • HCV E2 protein triggers the MAPK/ERK signaling pathway via CD81 and LDLR.
  • This signaling pathway activation by E2 promotes target cell survival and growth.
  • The findings provide insight into the molecular mechanisms of HCV-induced liver disease.

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