ArticleMolecular biology reports2026
Effect of Hepatitis B virus X T118N mutant protein in HepG2 cell cycle and apoptosis regulation.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundHepatitis B virus (HBV) belongs to Hepadnaviridae family and caused liver infection. HBV infection can develop into hepatocellular carcinoma, one of which is due to presence of HBV X protein (HBx). Some mutations are known to be associated with development of liver carcinoma, for instance HBx K130M/V131I (HBx_KV). In Indonesia, HBx T118N (HBx_T) has been found at similar frequency as the HBx_KV. This study aims to examine the effect of HBx T118N mutant on cell cycle and apoptosis regulation. METHODS AND
resultsIn this study, analysis of CyclinE, p21, Bax, and Bcl-2 gene expression was performed using RT-qPCR. Cell cycle and apoptosis analysis was done using flowcytometry with PI and Annexin V-PI staining, respectively. Caspase 3 activity assay was performed using CaspACE™ Colorimetric Assay Kit. The presence of HBx_T mutant increased CyclinE expression at 72 h post transfection, similarly to HBx_KV. Both Bax and Bcl-2 mRNA level were also increased HepG2 cells expressing HBx_T in comparison to HBx_KV expression at 72 h post transfection. HBx_T expression in HepG2 cells at 48 h post transfection caused increase of AnnexinV+/PI- and AnnexinV+/PI+ cell populations, as compared to HBx_wt expression.
conclusionsOur data suggests that HBx_T influences cell cycle and apoptosis regulation in slightly different mechanism to HBx_KV. Further investigations are still required to understand HBx_T mutant involvement in development of chronic liver disease and liver cirrhosis.
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