Metabolism-regulated ferroptosis in cancer progression and therapy

• Published in: Cell death & disease 2024-03, Vol.15 (3), p.196-196, Article 196
• Main Authors: Ye, Lvlan, Wen, Xiangqiong, Qin, Jiale, Zhang, Xiang, Wang, Youpeng, Wang, Ziyang, Zhou, Ti, Di, Yuqin, He, Weiling
• Format: Article
• Language: English
• Subjects: 631/67/2327; 631/80/82; 631/80/86; 96/95; Amino acids; Antibodies; Apoptosis; Autophagy; Biochemistry; Biomedical and Life Sciences; Cancer therapies; Carbohydrate metabolism; Carbohydrates; Cell Biology; Cell Culture; Cell death; Energy; Enzymes; Ferroptosis; Gastrointestinal surgery; Immunology; Immunotherapy; Kinases; Life Sciences; Lipid metabolism; Lipid peroxidation; Lipids; Metabolism; Metabolites; Microenvironments; Mysteries; Necroptosis; Polyunsaturated fatty acids; Pyroptosis; Review Article; Tumors
• ISSN: 2041-4889; 2041-4889
• DOI: 10.1038/s41419-024-06584-y

Cancer metabolism mainly includes carbohydrate, amino acid and lipid metabolism, each of which can be reprogrammed. These processes interact with each other to adapt to the complicated microenvironment. Ferroptosis is a regulated cell death induced by iron-dependent lipid peroxidation, which is morphologically different from apoptosis, necrosis, necroptosis, pyroptosis, autophagy-dependent cell death and cuprotosis. Cancer metabolism plays opposite roles in ferroptosis. On the one hand, carbohydrate metabolism can produce NADPH to maintain GPX4 and FSP1 function, and amino acid metabolism can provide substrates for synthesizing GPX4; on the other hand, lipid metabolism might synthesize PUFAs to trigger ferroptosis. The mechanisms through which cancer metabolism affects ferroptosis have been investigated extensively for a long time; however, some mechanisms have not yet been elucidated. In this review, we summarize the interaction between cancer metabolism and ferroptosis. Importantly, we were most concerned with how these targets can be utilized in cancer therapy.