Hepatitis B virus X protein blunts senescence‐like growth arrest of human hepatocellular carcinoma by reducing Notch1 cleavage

@article{Xu2010HepatitisBV,
  title={Hepatitis B virus X protein blunts senescence‐like growth arrest of human hepatocellular carcinoma by reducing Notch1 cleavage},
  author={Jiejie Xu and Xiao-jing Yun and Jianhai Jiang and Yuanyan Wei and Yi-hong Wu and Wei Zhang and Yeheng Liu and Wen-zhong Wang and Yu-mei Wen and Jianxin Gu},
  journal={Hepatology},
  year={2010},
  volume={52}
}
One of the serious sequelae of chronic hepatitis B virus (HBV) infection is hepatocellular carcinoma (HCC). Among all the proteins encoded by the HBV genome, hepatitis B virus X protein (HBx) is highly associated with the development of HCC. Although Notch1 signaling has been found to exert a tumor‐suppressive function during HCC development, the mechanism of interaction between HBx expression and Notch1 signaling needs to be explored. In this study, we report that HBx expression in hepatic and… 
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Hepatitis B virus X protein activates Notch signaling by its effects on Notch1 and Notch4 in human hepatocellular carcinoma.
TLDR
The present study indicates that HBx activates Notch signaling by its effects on Notch1 and Notch4, and therefore, recruits notch signaling as a downstream pathway contributing to its carcinogenic role in HBV-associated HCC.
Hepatitis B virus X protein activates Notch signaling by its effects on Notch 1 and Notch 4 in human hepatocellular carcinoma
TLDR
The present study indicates that HBx activates Notch signaling by its effects on Notch1 and Notch4, and therefore, recruits notch signaling as a downstream pathway contributing to its carcinogenic role in HBV-associated HCC.
Hepatitis B virus large surface antigen promotes liver carcinogenesis by activating the Src/PI3K/Akt pathway.
TLDR
It is suggested that LHBs promotes tumorigenesis of hepatoma cells by triggering a PKCα/Raf1 to Src/PI3K/Akt signaling pathway, revealing novel insights into the underlying mechanisms of HBV-associated hepatocarcinogenesis.
Hepatitis B virus X protein in the proliferation of hepatocellular carcinoma cells.
Hepatocellular carcinoma (HCC) is one of the most common and deadly malignant neoplasms worldwide. Chronic hepatitis B virus (HBV) infection is closely associated with the occurrence of HCC. The HBV…
Hepatitis B Virus Large Surface Antigen Promotes Liver Carcinogenesis by Activating the Src / PI 3 K / Akt Pathway
TLDR
It is suggested that LHBs promotes tumorigenesis of hepatoma cells by triggering a PKCa/Raf1 to Src/PI3K/Akt signaling pathway, revealing novel insights into the underlying mechanisms of HBVassociated hepatocarcinogenesis.
Hepatitis B virus X protein promotes hepatoma cell invasion and metastasis by stabilizing Snail protein
TLDR
A novel function of HBx is revealed in promoting epithelial–mesenchymal transition through Snail protein stabilization by activating PI3K/AKT/GSK‐3β signaling, thus facilitating tumor invasion and metastasis during HCC progression.
Hepatitis B Virus Large Surface Antigen Promotes Tumorigenesis of Human Hepatocellular Carcinoma Cells through Activating Src / PI 3 K / Akt Pathway
TLDR
It is proposed that LHBs could promote tumorigenesis of hepatoma cells dependent on PKC /Raf1/Src/PI3K/Akt signal activation, which reveals a novel insight into the underlying mechanisms for HBV-associated hepatocarcinogenesis.
Effects of hepatitis B virus X gene on apoptosis and expression of immune molecules of human proximal tubular epithelial cells
TLDR
Overexpression of the HBx gene in renal tubular epithelial cells induces apoptosis of HK-2 cells and promotes epithelial-mesenchymal transdifferentiation and induces an imbalance in cytokine levels.
Hepatitis B virus X protein confers resistance of hepatoma cells to anoikis by up-regulating and activating p21-activated kinase 1.
TLDR
The HBV protein HBx up-regulates PAK1, allows hepatoma cells to become resistant to anoikis, and promotes growth of aggressive xenograft tumors in mice.
USP16 Downregulation by Carboxyl-terminal Truncated HBx Promotes the Growth of Hepatocellular Carcinoma Cells
TLDR
This study suggests that USP16 downregulation is a critical event in Ct-HBx-mediated promotion of HCC tumorigenicity and malignancy.
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TLDR
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