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摘要
肝细胞癌(HCC)是世界上癌症导致死亡的主要因素。尤其是在西方国家。丙型肝炎病毒(HCV)感染是导致慢性肝病和肝癌的主要原因。多种分子机制参与了丙型肝炎病毒诱导肝细胞癌的发生和发展,其中氧化应激起着关键性的作用。过量的氧自由基直接损伤DNA、脂类和蛋白质。同时,活性氧间接激活一系列信号级联反应,调节许多转录因子的活性,导致控制细胞存活、增殖、血管生成、侵袭和转移的基因表达改变。丙型肝炎病毒感染导致活性氧过量生成,损害内源性抗氧化剂的功能。在这篇综述中,我们总结了丙型肝炎病毒感染的机体中氧化应激和肝癌之间的联系以及可能的分子机制,以探索丙型肝炎病毒诱导肝细胞癌可能的途径或干预的靶点。
关键词: 丙型肝炎病毒,氧化应激,活性氧,肝细胞癌,慢性肝病。
Current Cancer Drug Targets
Title:Role of Oxidative Stress in Hepatitis C Virus Induced Hepatocellular Carcinoma
Volume: 17 Issue: 6
关键词: 丙型肝炎病毒,氧化应激,活性氧,肝细胞癌,慢性肝病。
摘要: 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.
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Cite this article as:
Role of Oxidative Stress in Hepatitis C Virus Induced Hepatocellular Carcinoma, Current Cancer Drug Targets 2017; 17 (6) . https://dx.doi.org/10.2174/1568009616666160926124043
DOI https://dx.doi.org/10.2174/1568009616666160926124043 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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