ArticleBiochemistry and biophysics reports2020
EGF receptor inhibitors comprehensively suppress hepatitis B virus by downregulation of STAT3 phosphorylation.
Article in Biochemistry and biophysics reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- EGF rs4444903 polymorphism is associated with risk of HCV-related cirrhosis and HBV/HCV-related hepatocellular carcinoma.International journal of clinical oncology · 2021Pooled it
- Repurposing Product Nkabinde for Hepatitis B Virus Therapy: A Network Pharmacology and Molecular Docking Investigation.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Recent Progress in Treating Airway Mucus Hypersecretion by Targeting the Epidermal Growth Factor Receptor Signaling Pathway.Pediatric discovery · 2026Review
- MSP-RON signaling in liver pathobiology and as an emerging therapeutic target: a review of the current evidence.Cell communication and signaling : CCS · 2025Review
- STAT3 Increases CVB3 Replication and Acute Pancreatitis and Myocarditis Pathology via Impeding Nuclear Translocation of STAT1 and Interferon-Stimulated Gene Expression.International journal of molecular sciences · 2024Article
- De novo Hepatitis B Virus Reactivation during Treatment with an Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor in a Patient with Advanced Lung Cancer.Internal medicine (Tokyo, Japan) · 2024Article
- circRNA expression patterns and circRNA-miRNA-mRNA networks during CV-A16 infection of SH-SY5Y cells.Archives of virology · 2021Article
- The roles of signaling pathways in SARS-CoV-2 infection; lessons learned from SARS-CoV and MERS-CoV.Archives of virology · 2021Review
- Host directed therapies: COVID-19 and beyond.Current research in pharmacology and drug discovery · 2021Review
- Suppression of Interferon-α Treatment Response by Host Negative Factors in Hepatitis B Virus Infection.Frontiers in medicine · 2021Review
- Strategy, Progress, and Challenges of Drug Repurposing for Efficient Antiviral Discovery.Frontiers in pharmacology · 2021Review
- Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current antiviral therapy can not cure chronic hepatitis B virus (HBV) infection or eliminate the risk of hepatocellular carcinoma. The licensed epidermal growth factor receptor (EGFR) inhibitors have found to inhibit hepatitis C virus replication via downregulation of signal transducers and activators of transcription 3 (STAT3) phosphorylation. Since STAT3 is also involved in HBV replication, we further studied the anti-HBV efficacy of the EGFR inhibitors in this study. HBV-transfected HepG2.2.15 cells and HBV-infected HepG2-NTCP cells were used as cell models, and HBV replication, the syntheses of viral antigens and the magnitude of the covalently closed circular DNA (cccDNA) reservoir were used as indictors to test the anti-HBV effects of EGFR inhibitors erlotinib and gefitinib. Erlotinib inhibited HBV replication with a half-maximal inhibitory concentration of 1.05 μM. It also reduced the syntheses of viral antigens at concentrations of 2.5 μM or higher. The underlying mechanism was possibly correlated with its inhibition on STAT3 phosphorylation via up-regulation of suppressor of cytokine signaling 3. Gefitinib also inhibited HBV replication and antigen syntheses. Compared with the commonest antiviral drug entecavir, these EGFR inhibitors additionally reduced hepatitis B e antigen and erlotinib also marginally affected the cccDNA reservoir in HBV-infected HepG2-NTCP cells. Interestingly, these promising anti-HBV effects were significantly enhanced by extension of treatment duration. In conclusion, EGFR inhibitors demonstrated a comprehensive anti-HBV potential, highlighting a new strategy to cure HBV infection and suggesting animal model-related studies or clinical try in the future.
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