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Carcinogenesis Advance Access published online on April 2, 2007
Carcinogenesis, doi:10.1093/carcin/bgm075
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Published by Oxford University Press 2007.

Induction of a unique gene expression profile in primary human hepatocytes by hepatitis C virus core, NS3 and NS5A proteins

A Budhu1, Y Chen2, JW Kim1,*, M Forgues1, K Valerie3, CC Harris1 and XW Wang1,**

1 Laboratory of Human Carcinogenesis
2 Genetics Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892
3 Department of Radiation Oncology, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0058

** Corresponding author; 37 Convent Drive, Bldg. 37, Rm. 3044, Bethesda, MD 20892-4258; 301-496-2099; xw3u{at}nih.gov

Hepatocellular carcinoma (HCC) is a fatal disease and hepatitis B and C viruses (HBV and HCV) are considered major causative factors for the development of HCC. We have conducted gene expression profiling studies to search for potential target genes responsible for HCV-mediated HCC. Adenoviruses encoding core (HCV structural protein), NS3 and NS5A (HCV non-structural proteins) were generated and infected individually or together in freshly isolated primary human hepatocytes. An adenovirus harboring the oncogenic HBV protein, HBx was included for comparison. A microarray platform of over 22,000 human oligos was analyzed to seek out significant differentially expressed genes among these viral proteins. We also compared these gene expression profiles to those obtained from HCV-infected liver samples from chronic liver disease (CLD) patients and HCV-related HCC. We found that HCV-related proteins largely induce unique genes when compared to HBx. In particular, interferon-inducible gene 27 (IFI27) was highly expressed in HCV or core infected hepatocytes and HCV-related CLD or HCC, but was not less significantly expressed in HBx infected hepatocytes or HBV-related CLD or HCC, indicating that IFI27 may play a role in HCV-mediated HCC. In conclusion, our results suggest that HBV and HCV promote HCC development mainly through different mechanisms.

* Current address: Center for Human Genomics, Wake Forest University School of Medicine, Medical Center Blvd. Winston-Salem, NC 27157

Received February 1, 2007; revised March 26, 2007; accepted March 26, 2007.


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