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Ferroptosis and the risk of gastric cancer


 Ferroptosis and gastric cancer risk

Ferroptosis, an iron-dependent controlled form of cell death caused by lipid peroxide build-up, is linked to several disorders and exhibits a tumor suppressor function. Ferroptosis is a unique cell death modality triggered by iron-dependent lipid peroxidation, with cysteine metabolism and glutathione (GSH)-dependent antioxidant defense responses as the primary triggering mechanisms. In the specific, during the tumorigenesis, ferroptosis plays a dual role in promoting and inhibiting tumors. P53, NFE2L2, BAP1, HIF, and other tumor suppressor genes regulate ferroptosis, releasing damage-associated molecular patterns or lipid metabolites to influence cellular immune responses. Moreover, ferroptosis is also involved in tumor suppression and metabolism. The combination of amino acid, lipid, and iron metabolism is involved in the initiation and execution of ferroptosis, and metabolic regulatory mechanisms also play roles in malignancies. Most investigations into ferroptosis in gastric cancer are concentrated on predictive models, not the underlying processes, because it may play a role in the occurrence and development of gastric cancer. Many studies have linked ferroptosis to tumor incidence, growth, invasion, and metastasis, particularly in tumour microenvironment and immunotherapy studies.

Wang, Haibin