Dual effects of hepatitis B virus X protein on the regulation of cell-cycle control depending on the status of cellular p53.

Abstract	Despite the extensive studies on the roles of hepatitis B virus (HBV) X protein (HBx) in the development of hepatocellular carcinomas (HCCs), the mechanisms by which HBx contributes to HCC remain controversial. In this study, the effect of HBx on the G(1)-S checkpoint control depending on the status of p53 was compared. Transcription of p21(waf1/cip1) was activated by HBx in the presence of functional p53 in a dose-dependent manner. However, it was repressed by HBx when p53 was absent or present at a low level. Furthermore, the growth rate of the HBx-expressing NIH3T3 cell lines compared with that of the parental cells was decreased when p53 was upregulated by a DNA-damaging agent, cisplatin, whereas it increased approximately twofold when p53 was present at a very low level. Thus, the opposite effects of HBx on the regulation of the cell cycle depending on the status of p53 might be important to understand the progression of hepatic diseases in HBV-positive patients.
Authors	Ji Young Ahn, Eun Young Jung, Hyun Jin Kwun, Chang-Woo Lee, Young-Chul Sung, Kyung Lib Jang
Journal	The Journal of general virology (J Gen Virol) Vol. 83 Issue Pt 11 Pg. 2765-2772 (Nov 2002) ISSN: 0022-1317 [Print] England
PMID	12388812 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	CDKN1A protein, human Cdkn1a protein, mouse Cyclin-Dependent Kinase Inhibitor p21 Cyclins Repressor Proteins Trans-Activators Tumor Suppressor Protein p53 Viral Regulatory and Accessory Proteins hepatitis B virus X protein
Topics	3T3 Cells Animals Cell Cycle Cyclin-Dependent Kinase Inhibitor p21 Cyclins (genetics) Gene Expression Regulation Hepatitis B virus (metabolism) Humans Mice Repressor Proteins (metabolism) Trans-Activators (metabolism) Transcription, Genetic Tumor Cells, Cultured Tumor Suppressor Protein p53 (genetics, metabolism) Viral Regulatory and Accessory Proteins

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