Progressive changes in hepatoma cells stably transfected with hepatitis B virus X gene

Ye, L.; Dong, N.; Wang, Q.; Xu, Z.; Cai, N.; Wang, H.; Zhang, X.

Intervirology 51(1): 50-58

2008


ISSN/ISBN: 1423-0100
PMID: 18334850
DOI: 10.1159/000120289
Accession: 021610286

Download citation:  
Text
  |  
BibTeX
  |  
RIS

Article/Abstract emailed within 0-6 h
Payments are secure & encrypted
Powered by Stripe
Powered by PayPal

Abstract
The aim of this study is to investigate the molecular mechanism of hepatocellular carcinoma (HCC) development induced by hepatitis B virus X protein (HBx). We previously established a H7402-X cell line that constitutively expresses HBx protein. In the present study, H7402-X gene expression profiles and proteins were examined using cDNA microarrays and Western blot analysis. Apoptosis was induced by adriamycin in H7402-X cells. The transcriptional activities of NF-kappaB and AP-1 were examined using a luciferase reporter gene. The DNA expression profiles identified candidate genes showing aberrant expression in cells overexpressing HBx. Western blot analysis showed that cyclin D, cyclin E, survivin, Bcl-2, and PCNA were up-regulated, whereas p27 was down-regulated in H7402-X cells. Treatment with RNAi targeting HBx mRNA led to the down-regulation of these genes. H7402-X cells were resistant to adriamycin-induced apoptosis. Luciferase reporter gene analysis revealed that HBx induces the transcriptional activities of NF-kappaB and AP-1. Our data provide additional insight into cellular targets of HBx, which allows a better understanding of HBx function and the progressive changes during HBx-mediated hepatocarcinogenesis.