Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Feb 21;11(4):741.
doi: 10.3390/cells11040741.

Hepatitis B Viral Protein HBx and the Molecular Mechanisms Modulating the Hallmarks of Hepatocellular Carcinoma: A Comprehensive Review

Affiliations
Review

Hepatitis B Viral Protein HBx and the Molecular Mechanisms Modulating the Hallmarks of Hepatocellular Carcinoma: A Comprehensive Review

Enakshi Sivasudhan et al. Cells. .

Abstract

With 296 million cases estimated worldwide, chronic hepatitis B virus (HBV) infection is the most common risk factor for hepatocellular carcinoma (HCC). HBV-encoded oncogene X protein (HBx), a key multifunctional regulatory protein, drives viral replication and interferes with several cellular signalling pathways that drive virus-associated hepatocarcinogenesis. This review article provides a comprehensive overview of the role of HBx in modulating the various hallmarks of HCC by supporting tumour initiation, progression, invasion and metastasis. Understanding HBx-mediated dimensions of complexity in driving liver malignancies could provide the key to unlocking novel and repurposed combinatorial therapies to combat HCC.

Keywords: HBx protein; cancer hallmarks; hepatitis B virus; hepatocellular carcinoma; therapeutics.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Hallmarks of hepatocellular carcinoma modulated by hepatitis B virus X protein (HBx). Numerous liver tumorigenesis-driving hallmarks influence the downstream cellular mechanisms by sustaining proliferative signalling, eluding growth suppressors, evading immune destruction, facilitating replicative immortality, aiding in tumour-promoting inflammation, triggering invasion and metastasis, prompting angiogenesis, inducing genome instability, preventing cell apoptosis, and deregulating cellular energetics.

References

    1. World Health Organization Global Progress Report on HIV, Viral Hepatitis and Sexually Transmitted Infections. 2021. [(accessed on 29 December 2021)]. Available online: https://www.who.int/publications/i/item/9789240027077.
    1. Wong V.W.-S., Janssen H.L.A. Can we use hcc risk scores to individualize surveillance in chronic hepatitis b infection? J. Hepatol. 2015;63:722–732. doi: 10.1016/j.jhep.2015.05.019. - DOI - PubMed
    1. Sung H., Ferlay J., Siegel R.L., Laversanne M., Soerjomataram I., Jemal A., Bray F. Global cancer statistics 2020: Globocan estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J. Clin. 2021;71:209–249. doi: 10.3322/caac.21660. - DOI - PubMed
    1. Kgatle M. Advances in Treatment of Hepatitis C and B. IntechOpen; London, UK: 2017. Recent advancement in hepatitis b virus, epigenetics alterations and related complications.
    1. Seeger C., Mason W.S. Hepatitis b virus biology. Microbiol. Mol. Biol. Rev. MMBR. 2000;64:51–68. doi: 10.1128/MMBR.64.1.51-68.2000. - DOI - PMC - PubMed

Publication types

MeSH terms

Substances