The role of non-coding RNA in ferroptosis of liver cancer and its impact on lipid peroxidation.

Ferroptosis is an iron-dependent programmed death caused by the imbalance of lipid peroxides in cells. Unlike apoptosis, autophagy and necrosis, ferroptosis is mainly induced by the small molecule compound erastin. The main characteristics of ferroptosis were glutathione (GSH) depletion, inactivation of glutathione peroxidase 4 (GPX4) and reactive oxygen species (ROS) promoting lipid peroxidation. Eventually, the imbalance of lipid peroxidation regulation in cells leads to ferroptosis. The lipid metabolic pathway ultimately contributes to ferroptosis through the production of lipid peroxides. In addition, other cellular metabolic pathways can also regulate ferroptosis, such as the antioxidant metabolic pathway, which inhibits ferroptosis by clearing lipid peroxides and reducing cell membrane damage. Long non-coding RNAs (lncRNAs) are non-coding transcripts more than 200 nucleotides in length and are a less classified group of RNA transcripts that are associated with tumorigenesis and metastasis and are more tissue or cell type specific than protein-coding genes. Studies on the molecular profile of lncRNAs in plasma samples from liver cancer patients show that differentially expressed lncRNAs are mainly concentrated in biological functions related to tumorigenesis, such as cell metastasis, immune response and metabolic regulation. With different biological functions in physiological and pathological environments, the specific expression patterns of lncRNAs coordinate cell state, development, differentiation, and disease.