Regulation of HepG2 cell apoptosis by hepatitis C virus (HCV) core protein via the sirt1–p53–bax pathway
- 381 Downloads
Hepatitis C virus (HCV) core protein stimulates many signaling pathways related to apoptosis inhibition resulting in hepatocellular carcinoma (HCC). It has been reported that sirt1 is involved in regulating apoptosis; therefore, we investigated the influence of HCV core protein on sirt1 expression and apoptosis in human HepG2 cells. Our study showed that HCV core protein inhibited apoptosis of HepG2 cells as well as caspase-3 expression and activity (P < 0.05). At the same time, sirt1 expression was increased at both the mRNA (P < 0.05) and protein (P < 0.05) levels. Furthermore, apoptosis inhibition was reversed when sirt1 was knocked down (P < 0.05). Our study provides further evidence that the sirt1–p53–Bax signaling pathway plays an important role in regulating the suppression of cell apoptosis induced by HCV core protein.
KeywordsHCV core Apoptosis sirt1 p53 Bax
This work was supported by grants from the Healthy Talent Leadership Programs of Beijing (Nos. 2009-1-09), and the National Key Projects of Infectious Diseases during the Five-Year Plan Period of China (Nos. 2012ZX10002003, 2013ZX10002005 and 2012ZX10004904). We would like to express our gratitude to all the members in our group, Beijing Key Laboratory of Emerging Infectious Diseases, for supportive discussions and technical assistance.
Jun Cheng contributed to the study design, data analysis, and critical review of the manuscript. Shenghu Feng was involved in the entire study, conducting the experiments, analyzing and interpreting the data, and drafting the manuscript. Min Li contributed to the study design and data collection. Qi Wang, Shunai Liu, and Jinqian Zhang contributed to study design. Min Quan and Yu Zhang contributed the technical assistance. All authors finalized the manuscript and have read and approved the final draft.
Compliance with ethical standards
The authors declare that they have no financial interests related to the material in the manuscript.