The unique role of the hepatitis virus B X protein on HEK 293 cell morphology and cellular change
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The function of the hepatitis B virus X protein (HBx) has been investigated in hepatoma cell lines before; however, its function in the canonical HEK 293 cell line has not been addressed. In this study, we found that HBx increased cellular interaction by fusing the gap between HEK 293 cells, which is different from what has been reported previously. We also found that HBx enhanced the expression of E-cadherin in hepatoma cell lines instead of decreasing it as reported previously. The increase in E-cadherin was mediated by the enhanced levels of Src, which also differs from previous reports. Finally, we observed that HBx can accelerate cell growth by increasing the percentage of cells that are positioned at the division stage. Further analysis showed that the increased growth was caused by increased CDK4 expression and Ki67+ populations. Additionally, reduced apoptosis was found in HEK 293 cells expressing HBx due to an increase in the anti-apoptotic protein-Bcl2. Collectively, the different functions of HBx in HEK 293 cells suggest that its role is cell dependent.
KeywordsHepG2 Cell CDK4 Expression Chang Liver Cell Western Blot Profile Centrosome Dynamic
We thank Drs. Vera Stupina and Megan Young for critically reading the manuscript. This work was supported by a project from Chongqing Science and Technology Commission (cstc2015shmszx0196). The authors have no conflicts of interest to declare. This article does not contain any studies with human participants or animals performed by any of the authors.
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