Exploring the Therapeutic Potential of Ferroptosis in Gastric Cancer

Ferroptosis refers to the regulatory cell death type with the typical feature of iron-dependent lipid peroxidation (LPO), which has been implicated in various aspects of cancer development and progression. Ferroptosis dysregulation can promote the occurrence, metastasis, and therapy resistance of gastric cancer (GC). Understanding the ferroptosis-related molecular mechanisms in GC progression could lead to novel therapeutic strategies that target this pathway. This review briefly introduces the mechanisms of ferroptosis and concludes that targeting ferroptosis can regulate the sensitivity of GC cells to chemotherapy resistance and immunotherapy. Natural plant extracts and traditional medicine play a key role in the treatment of GC by inducing ferroptosis through pathways such as activating p53 and inhibiting nuclear factor erythrocyte 2-related factor 2 (NRF2). Additionally, novel nanoparticle materials can be used as a drug carrier to promote ferroptosis while suppressing GC cell or gastric cancer stem cell (GCSC) growth, providing a novel direction for treating GC. It also summarizes other drugs such as 6-Thioguanine, Polymerase theta, levobupivacaine and clinical application drugs, which target ferroptosis, the effect of them in treating GC. This review highlights the potential of ferroptosis induction in GC treatment, providing new avenues for clinical intervention. Finally, this review looks forward to the translational prospects of targeting ferroptosis in the development of GC treatment, offering key insights for future research directions and therapeutic strategies.