Gene Expression Profile in Response to Hepatitis B Virus X Gene by Using an Adenoviral Vector.
- Author:
Heui Yun JOO
1
;
Kwang Hyub HAN
;
Wang Shick RYU
Author Information
1. National Research Laboratory of Tumor Virology, Yonsei University, Seoul, Korea. wsryu@yonsei.ac.kr
- Publication Type:Original Article ; English Abstract
- Keywords:
Hepatitis B Virus/Hepatitis B virus X gene;
Recombinant adenovirus;
cDNA microarray
- MeSH:
Carcinoma, Hepatocellular/*virology;
Cell Line, Tumor;
English Abstract;
*Gene Expression Profiling;
Gene Expression Regulation;
Genes, Viral/*physiology;
Genetic Vectors;
Hepatitis B Antigens/genetics;
Hepatitis B Virus/*genetics;
Human;
Liver Neoplasms/*virology;
Oligonucleotide Array Sequence Analysis;
Trans-Activators/*genetics/physiology
- From:The Korean Journal of Hepatology
2002;8(4):371-380
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND/AIMS: Hepatitis B virus (HBV) is the etiological factor for hepatocellular carcinoma (HCC). Numerous evidence has indicated a link between chronic infection with HBV and the development of HCC. Among the four proteins encoded by HBV, Hepatitis B virus X gene(HBx), best characterized as a transcriptional transactivator, gained attention owing to its presumptive role in oncogenesis. Further, HBx has been shown to stimulate signal transduction pathways such as Ras-MAPK pathway, NF-kappaB, and Src kinase. The pleiotropic events caused by HBx may be the key to understanding the HBV-mediated oncogenicity. However, the specific roles of HBx in oncogenesis remain largely elusive. To explore the role of HBx in hepatocarcinogenesis, we examined the deregulation of host genes induced by HBx expression. METHODS: HBx was ectopically expressed in HepG2 cells using a recombinant adenovirus to transiently express HBx. Gene expression profiling of HBx was conducted on cDNA microarrays that contained 1,028 cDNAs. RESULTS: A number of oncogenes and genes that are involved in cell growth, DNA repair, cell cycle regulation, and cell motility were deregulated by HBx. CONCLUSIONS: Theses results suggest that HBx regulates transcription in a way that contributes to the proliferation of hepatocytes, a probable early event of HCC.
