Hepatitis B virus X protein suppresses all-trans retinoic acid-induced apoptosis in human hepatocytes by repressing p14 expression via DNA methylation.

@article{Choi2017HepatitisBV,
  title={Hepatitis B virus X protein suppresses all-trans retinoic acid-induced apoptosis in human hepatocytes by repressing p14 expression via DNA methylation.},
  author={Jung-Hye Choi and Hyerin Jeong and Kyung Lib Jang},
  journal={The Journal of general virology},
  year={2017},
  volume={98 11},
  pages={
          2786-2798
        }
}
All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to activate p14 expression via promoter hypermethylation to induce p53-dependent apoptosis in human hepatocytes. In this study, we found that the oncogenic hepatitis B virus (HBV) X protein (HBx) of HBV, derived from both overexpression and 1.2-mer replicon systems, suppresses ATRA-induced apoptosis in p53-positive human hepatocytes. For this effect, HBx upregulated both protein and enzyme activity… 
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TLDR
HBx, the principal oncogene product of HBV, induced promoter hypermethylation of RAR-beta(2) via upregulation of DNA methyltransferases 1 and 3a, resulting in downregulation of its expression in human HCC cells, and HBx-expressing cells were less susceptible to RA-induced cell growth inhibition compared with control cells.
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TLDR
It is shown that hepatitis B virus (HBx) overcomes cellular senescence provoked by all-trans retinoic acid (ATRA) in HepG2 cells, and HBx suppressed ATRA-mediated induction of p16 and p21 in Hepg2 cells via promoter hypermethylation, resulting in inactivation of retinoblastoma protein.
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TLDR
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TLDR
It is reported that HBV X protein (HBx) represses E-cadherin expression at the transcription level by inducing methylation-mediated promoter inactivation and suggests that HBx plays a role during hepatocellular carcinogenesis by favoring cell detachment from the surrounding cells and migration outside of the primary tumor site.
Hepatitis B Virus X Protein via the p38MAPK Pathway Induces E2F1 Release and ATR Kinase Activation Mediating p53 Apoptosis*
TLDR
It is demonstrated that the p38MAPK pathway activated by pX serves this role in p53 apoptosis, which couples p53 stabilization and p53 activation, by E2F1 induction and ATR activation, respectively.
X Protein of Hepatitis B Virus Inhibits Fas-mediated Apoptosis and Is Associated with Up-regulation of the SAPK/JNK Pathway*
TLDR
Experiments demonstrated that cell death caused by anti-Fas antibodies was blocked by the expression of HBx in human primary hepatocytes and mouse embryo fibroblasts, indicating that protection against Fas-mediated apoptosis was independent of p53.
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TLDR
The results indicate that, unlike other DNA tumor viruses that block apoptosis by inactivating p53, the hepatitis B virus achieves protection from apoptotic death through a HBx-PI3K-Akt-Bad pathway and by inActivating caspase 3 activity that is at least partially p53-independent in liver cells.
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TLDR
It is shown that hepatitis B virus X protein (HBx) activates DNMT1 expression via a regulatory circuit involving the p16(INK4a)-cyclin D1-cyclin-dependent kinase (CDK) 4/6-retinoblastoma protein (pRb)-E2F1 pathway, and that accumulatedDNMT1 via this pathway inactivates E-cadherin expression through promoter hypermethylation.
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