Next Article in Journal
Molecular Mechanisms of RADA16-1 Peptide on Fast Stop Bleeding in Rat Models
Next Article in Special Issue
Microtubule Formation and Activities of Antioxidative Enzymes in PC12 Cells Exposed to Phosphatidylcholine Hydroperoxides
Previous Article in Journal
Simple Estimation of Förster Resonance Energy Transfer (FRET) Orientation Factor Distribution in Membranes
Previous Article in Special Issue
Oxidant Stress and Signal Transduction in the Nervous System with the PI 3-K, Akt, and mTOR Cascade
Article Menu

Export Article

Open AccessReview
Int. J. Mol. Sci. 2012, 13(11), 15271-15278; doi:10.3390/ijms131115271

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
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)
View Full-Text   |   Download PDF [225 KB, uploaded 19 June 2014]   |  


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.
Keywords: hepatitis C virus; reactive oxygen species; 3β-hydroxysterol ∆24-reductase hepatitis C virus; reactive oxygen species; 3β-hydroxysterol ∆24-reductase
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

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.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top