| Liver cancer is one of the leading causes of cancer-related deaths globally, significantly affecting patients' quality of life and survival rates. Despite advancements in modern medicine, the treatment of liver cancer still faces numerous challenges and limitations, making the search for new therapeutic strategies of great clinical significance. Ferroptosis and cuproptosis have garnered considerable attention in liver cancer research in recent years. Ferroptosis, driven by iron-dependent lipid peroxidation, regulates liver cancer through multiple pathways, inhibiting its proliferation and metastasis. Cuproptosis is triggered by intracellular copper accumulation, involving the aggregation of mitochondrial lipoylated proteins and the degradation of iron-sulfur cluster proteins. Excess copper ions interfere with the respiratory chain complexes, causing protein toxicity stress responses and inhibiting the proliferation of liver cancer cells. Ferroptosis and cuproptosis are interconnected in liver cancer, forming an interactive network centered around GSH and P53, offering potential for multi-target regulation of liver cancer. This review summarizes the mechanisms and interconnections of ferroptosis and cuproptosis in liver cancer, discusses their clinical application prospects in liver cancer treatment, and provides valuable references for further research and clinical practice. |
