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Abstrait
Role of Hepatitis B virus X Protein in DNA Repair During Hepatocellular Carcinoma Development
Hany A. Abdel-Hafiz
Hepatocellular carcinoma (HCC) is the most lethal cancer in the world. Hepatitis B virus (HBV), hepatitis C virus (HCV), alcohol intake, and aflatoxin-B exposure have been identified as distinct causative factors for HCC. HBV infections play an important role in the development of HCC. HBV X protein (HBx) is a multifunctional protein that can modulate various cellular processes and plays a crucial role in the pathogenesis of HCC. HBx protein promotes cell cycle progression, inactivates negative growth regulators, and inhibits tumor suppressor genes such as p53. It has been shown recently that HBx modulates transcription of methyltransferases, causing regional hypermethylation of DNA that result in silencing of tumor suppressor genes. HBx is known to interact with DNA helicase components of transcription factor IIH (TFIIH), a basal transcriptional factor and an integral component of DNA excision repair results in interference of nucleotide excision repair. This review focuses on the role of HBx in DNA damage repair as well as its involvement in the regulation of various signaling pathways.