role of oxidative stress in hepatocarcinogenesis induced by hepatitis c virus氧化应激在hepatocarcinogenesis丙型肝炎病毒引起的.pdfVIP

Int. J. Mol. Sci. 2012, 13, 15271-15278; doi:10.3390/ijms131115271 OPEN ACCESS International Journal of Molecular Sciences ISSN 1422-0067 /journal/ijms Review Role of Oxidative Stress in Hepatocarcinogenesis Induced by Hepatitis C Virus Kyoko Tsukiyama-Kohara Department of Animal Hygiene, Transboundary Animal Diseases Center, Joint Faculty of Veterinary Medicine Kagoshima University, 1-21-24 Korimoto, Kagoshima 890-0065, Japan; E-Mail: kkohara@agri.kagoshima-u.ac.jp; Tel./Fax: +81-99-285-3589 Received: 11 September 2012; in revised form: 8 November 2012 / Accepted: 9 November 2012 / Published: 19 November 2012 Abstract: Hepatitis C virus (HCV) easily establishes chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). During the progression of HCV infections, reactive oxygen species (ROS) are generated, and these ROS then induce significant DNA damage. The role of ROS in the pathogenesis of HCV infection is still not fully understood. Recently, we found that HCV induced the expression of 3β-hydroxysterol ∆24-reductase (DHCR24). We also found that a HCV responsive region is present in the 5-flanking genomic promoter region of DHCR24 and the HCV responsive region was characterized as (−167/−140). Moreover, the transcription factor Sp1 was found to bind to this region in response to oxidative stress under the regulation of ataxia telangiectasia