| Literature DB >> 27677955 |
Na Fu1, Hui Yao2, Yuemin Nan3, Liang Qiao4.
Abstract
Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death worldwide. Hepatitis C virus (HCV) infection is the predominant cause of chronic liver diseases and HCC, particularly in Western countries. Multiple molecular mechanisms are involved in the development and progression of HCV-related HCC, of which oxidative stress plays a pivotal role. HCV infection induces overproduction of reactive oxygen species (ROS) and impairs the function of endogenous antioxidants. Excessive amount of ROS directly damages DNA, lipids and proteins. Meanwhile, ROS indirectly activates a series of signaling cascades, and modulates the activity of many transcription factors, resulting in altered expression of genes that control cell survival, proliferation, angiogenesis, invasion and metastasis. In this review, we aim to summarize the possible molecular mechanisms underlying the link between the oxidative stress and hepatocarcinogenesis in HCV-infected individuals, in order to facilitate discovery of possible approaches or interventional targets for HCV-related HCC. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.Entities:
Keywords: Hepatitis C virus; chronic liver diseases; hepatocellular carcinoma; oxidative stress; reactive oxygen species
Mesh:
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Year: 2017 PMID: 27677955 DOI: 10.2174/1568009616666160926124043
Source DB: PubMed Journal: Curr Cancer Drug Targets ISSN: 1568-0096 Impact factor: 3.428