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Updated: Jul 16, 2025

Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle
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Published on: February 1, 2017

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The hepatitis B virus pre-core protein p22 suppresses TNFα-induced apoptosis by regulating the NF-κB pathway

Zhihong Diao1, Huan Luo1, Ying Li1

  • 1Department of Laboratory Medicine, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine Nanning 530011, Guangxi, P. R. China.

American Journal of Translational Research
|September 11, 2023
PubMed
Abstract

Insights

Hepatitis B virus protein p22 (HBV-p22) inhibits apoptosis in liver cancer cells by suppressing JNK signaling and activating the NF-κB pathway. This involves HBV-p22 interacting with and phosphorylating IKKα, offering potential therapeutic targets for hepatocellular carcinoma.

Area of Science:

  • Hepatology
  • Molecular Biology
  • Virology

Background:

  • Cell apoptosis is closely linked to hepatocellular carcinoma (HCC) progression.
  • Understanding viral interference with apoptosis is crucial for developing anti-cancer therapies.

Purpose of the Study:

  • To investigate the role of Hepatitis B virus e antigen-associated protein 22 (HBeAg-p22), also known as HBV-p22, in tumor necrosis factor-alpha (TNFα)-induced apoptosis.
  • To elucidate the molecular mechanisms by which HBV-p22 influences apoptotic pathways in liver cancer cells.

Main Methods:

  • Western blot analysis for protein expression.
  • Cell Counting Kit-8 (CCK8) for cell viability assays.
  • Flow cytometry for apoptosis assessment.
  • Co-immunoprecipitation and GST pull-down assays for protein-protein interactions.

Main Results:

  • HBV-p22 was found to inhibit apoptosis in human hepatoma cell lines following TNFα stimulation.
  • Mechanistically, HBV-p22 suppressed Jun N-terminal kinase (JNK) signaling pathways.
  • HBV-p22 enhanced nuclear factor kappa-B (NF-κB) signaling and interacted with I-kappa B kinase α (IKKα), increasing its phosphorylation.

Conclusions:

  • HBV-p22 exhibits an anti-apoptotic effect in hepatocellular carcinoma cells.
  • The anti-apoptotic mechanism involves the regulation of the NF-κB pathway through enhanced IKKα phosphorylation.
  • These findings highlight HBV-p22 as a potential target for HCC therapeutic strategies.
Keywords:
HBeAg-p22Hepatitis B virusNF-κB signalingTNFαapoptosishepatocellular carcinoma

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