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Role of Oxidative Stress in Hepatocarcinogenesis Induced by Hepatitis C Virus

Department of Animal Hygiene, Transboundary Animal Diseases Center, Joint Faculty of Veterinary Medicine Kagoshima University, 1-21-24 Korimoto, Kagoshima 890-0065, Japan
Int. J. Mol. Sci. 2012, 13(11), 15271-15278;
Received: 11 September 2012 / Revised: 8 November 2012 / Accepted: 9 November 2012 / Published: 19 November 2012
(This article belongs to the Special Issue Oxidative Stress and Ageing)
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 mutated (ATM) kinase. Overexpression of DHCR24 impaired p53 activity by suppression of acetylation and increased interaction with MDM2. This impairment of p53 suppressed the hydrogen peroxide-induced apoptotic response in hepatocytes. Thus, a target of oxidative stress in HCV infection is DHCR24 through Sp1, which suppresses apoptotic responses and increases tumorigenicity. View Full-Text
Keywords: hepatitis C virus; reactive oxygen species; 3β-hydroxysterol ∆24-reductase hepatitis C virus; reactive oxygen species; 3β-hydroxysterol ∆24-reductase
MDPI and ACS Style

Tsukiyama-Kohara, K. Role of Oxidative Stress in Hepatocarcinogenesis Induced by Hepatitis C Virus. Int. J. Mol. Sci. 2012, 13, 15271-15278.

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