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.