Department of Traditional and Western Medical Hepatology, The Third Hospital of Hebei Medical University, Shijiazhuang 050051, China.
The Second Department of General Surgery, The Second People's Hospital of Lanzhou City, Lanzhou 730046, China.
Curr Cancer Drug Targets. 2017;17(6):498-504. doi: 10.2174/1568009616666160926124043.
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.
肝细胞癌 (HCC) 是全球癌症相关死亡的主要原因。丙型肝炎病毒 (HCV) 感染是慢性肝病和 HCC 的主要病因,尤其是在西方国家。多种分子机制参与了 HCV 相关 HCC 的发生和发展,其中氧化应激起着关键作用。HCV 感染诱导活性氧 (ROS) 的过度产生,并损害内源性抗氧化剂的功能。过量的 ROS 会直接损伤 DNA、脂质和蛋白质。同时,ROS 还会间接激活一系列信号级联反应,并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发生改变。在这篇综述中,我们旨在总结 HCV 感染个体中氧化应激与肝癌发生之间可能存在的分子机制,以便为发现可能的治疗方法或干预靶点提供依据。