Research Progress on Ferroptosis in the Occurrence, Development and Treatment of Hepatocellular Carcinoma
TL;DR
This paper systematically summarizes the molecular regulatory mechanisms of ferroptosis in HCC, including abnormal alterations in core pathways such as iron metabolism, lipid peroxidation, and glutathione peroxidase 4 (GPX4), as well as its regulatory effects on tumor proliferation, metastasis, and the immune microenvironment.
Abstract
: Hepatocellular carcinoma (HCC) is [1] the most common and most lethal primary liver cancer globally, characterized by complex pathogenesis, difficult early diagnosis, frequent therapeutic resistance, and poor overall prognosis. As a novel iron-dependent form of programmed cell death, ferroptosis has attracted extensive attention in the field of tumor biology in recent years. This paper systematically summarizes the molecular regulatory mechanisms of ferroptosis in HCC, including abnormal alterations in core pathways such as iron metabolism, lipid peroxidation, and glutathione peroxidase 4 (GPX4), as well as its regulatory effects on tumor proliferation, metastasis, and the immune microenvironment. Meanwhile, this review focuses on the potential value of ferroptosis in reversing therapeutic resistance in HCC. In addition, this paper also summarizes the application prospects of ferroptosis-related gene-based biomarkers in the diagnosis and prognostic evaluation of HCC, as well as the latest research progress of ferroptosis-targeting therapeutic strategies (such as GPX4 inhibitors, system xc⁻ inhibitors, iron n anomedicines, etc.), providing new ideas and potential intervention targets for the precise treatment of HCC.