Document Detail

Transactivation of human alpha-fetoprotein gene by X-gene product of hepatitis B virus in human hepatoma cells.
MedLine Citation:
PMID:  11891535     Owner:  NLM     Status:  MEDLINE    
The X-gene product of hepatitis B virus (HBX) modulates a variety of viral and cellular genes relevant to hepatocarcinogenesis, where alpha-fetoprotein (AFP) is produced by hepatoma cells. In the present study, the possible mechanism by which HBX regulates AFP expression was investigated using three human hepatoma cells, HepG2, HuH-7 and Hep3B, which are known to contain the wild-type, the mutant-type and the deletion of p53, respectively. Transfection with the HBX expression vector stimulated the co-transfected AFP reporter gene expression in HepG2 cells and HuH-7 cells, but not in Hep3B cells. Transfection with the p53 expression vector repressed the AFP reporter gene expression in all three hepatoma cells, while overexpression of HBX counteracted the p53-induced repression. In addition, a G-->A substitution at nucleotide -119 in the AFP promoter sequence abrogated the stimulatory effect of HBX on the AFP promoter in HepG2 cells. These results suggest that HBX interacts with p53 to up-regulate AFP gene transcription probably by restoration of the p53-mediated repression of the AFP promotor activity.
Tetsuhiko Arima; Kazuhiko Nakao; Keisuke Nakata; Hiroki Ishikawa; Tatsuki Ichikawa; Keisuke Hamasaki; Nobuko Ishii; Katsumi Eguchi
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  International journal of molecular medicine     Volume:  9     ISSN:  1107-3756     ISO Abbreviation:  Int. J. Mol. Med.     Publication Date:  2002 Apr 
Date Detail:
Created Date:  2002-03-13     Completed Date:  2002-07-17     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9810955     Medline TA:  Int J Mol Med     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  397-400     Citation Subset:  IM    
First Department of Internal Medicine, Nagasaki University School of Medicine, Sakamoto, Nagasaki, Japan.
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MeSH Terms
Carcinoma, Hepatocellular / genetics*,  metabolism
Gene Expression Regulation, Neoplastic*
Liver Neoplasms / genetics*,  metabolism
Trans-Activators / genetics*,  metabolism
Transcriptional Activation*
Tumor Cells, Cultured
Tumor Suppressor Protein p53 / metabolism
alpha-Fetoproteins / genetics*,  metabolism
Reg. No./Substance:
0/Trans-Activators; 0/Tumor Suppressor Protein p53; 0/alpha-Fetoproteins; 0/hepatitis B virus X protein

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