Oxidative stress (OS) is linked to hepatocellular carcinoma (HCC) progression.
HCC may develop as a result of genetic changes, including oxidative injury to
both nuclear and mitochondrial DNA. Signaling pathways regulated by OS, such as
Wnt/-catenin and Notch pathways, are vital regulators in developing HCC.
OS-mediated activation of transcription factors, including nuclear
factor-B and p53, among others, is capable of regulating the redox
state of HCC cells. OS also affects the tumor microenvironment, which, in turn,
regulates HCC progression. In HCC, reactive oxygen species (ROS) can potentially
enhance tumor cell proliferation, metastasis, and resistance to treatment.
However, elevated ROS levels can cause cytotoxicity and trigger apoptosis in HCC
cells. This review highlights and explores potential oxidative stress-related
treatment targets in HCC, offering novel insights for clinical therapies.