Ferroptosis is a type of regulated cell death dependent on iron and reactive oxygen species. Ferroptosis is distinct from other cell death modalities, including apoptosis, autophagy and necrosis. Dysregulated ferroptosis has been implicated in a number of diseases, including neuropathy, ischemia reperfusion injury, acute kidney failure and cancer. The digestive system consists of several organs. The morbidity and mortality rates of digestive system cancer are high. The current review summarizes the role of ferroptosis in digestive system cancer. A large number of molecules, including tumor protein p53, retinoblastoma protein, nuclear factor E2-related factor 2, KH RNA binding domain containing signal transduction associated 1, cysteine dioxygenase type 1, metallothionein-1G, nuclear receptor coactivator 4, CDGSH iron sulfur domain 1, heat shock protein family A (Hsp70) member 5 and acyl-CoA synthetase long chain family member 4, regulate ferroptosis in digestive system cancer. Drugs such as cisplatin, baicalein, haloperidol, artesunate, piperlongumine, saponin and bromelain may cause cancer cell death by inducing ferroptosis. An improved understanding of ferroptosis in digestive system cancer may give rise to novel diagnostic and making therapeutic strategies.
Keywords: digestive cancer; ferroptosis; regulated cell death.