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Related Experiment Video

Updated: Dec 14, 2025

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HBx increases EGFR expression by inhibiting miR129-5p function.

Masanori Ochi1, Motoyuki Otsuka1, Reo Maruyama2

  • 1Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.

Biochemical and Biophysical Research Communications
|July 25, 2020
PubMed
Summary
This summary is machine-generated.

Hepatitis B virus (HBV) RNA can persist during treatment by hijacking a host microRNA (miRNA), miR129-5p. This viral mechanism promotes cell growth and may explain ongoing HBV pathogenicity despite antiviral therapy.

Keywords:
EGFRHBVZBTB20microRNA

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Area of Science:

  • Virology
  • Molecular Biology
  • Hepatology

Background:

  • Nucleos(t)ide analogs effectively suppress hepatitis B virus (HBV) replication but do not eliminate the viral covalently closed circular DNA (ccDNA).
  • Persistent HBV RNA transcription from ccDNA contributes to ongoing viral activity and potential pathogenicity during therapy.

Purpose of the Study:

  • To investigate the molecular mechanisms by which HBV RNA may maintain pathogenicity during nucleos(t)ide analog therapy.
  • To explore the interaction between HBV RNA, host microRNAs, and cellular pathways involved in viral persistence.

Main Methods:

  • Sequence analysis to identify similarities between HBV RNA and host microRNAs.
  • Functional assays to assess the impact of HBV X protein (HBx) on microRNA function and target gene expression.
  • Analysis of microRNA levels within Ago2-containing complexes to evaluate sequestration by viral RNA.

Main Results:

  • HBV RNA sequences, including those encoding HBx, share similarities with the host microRNA miR129-5p.
  • HBx inhibits miR129-5p function, leading to increased expression of ZBTB20, a miR129-5p target gene.
  • ZBTB20 activation of transcription and EGFR levels promotes cell growth, an effect reversed by ZBTB20 knockdown.
  • HBx expression reduces miR129-5p levels in Ago2 complexes, suggesting viral RNA sequestration.

Conclusions:

  • HBV RNA can sequester miR129-5p, disrupting its regulatory function and promoting cellular pathways that enhance cell growth.
  • This viral RNA-mediated mechanism offers a potential explanation for the continued pathogenicity of HBV during nucleos(t)ide analog therapy.
  • Targeting the interaction between HBV RNA and host miRNAs could represent a novel therapeutic strategy for HBV infection.