Progress in research on the mechanisms and therapeutic strategies of SLC7A11 regulation in glioma

This review summarizes the critical role of SLC7A11 in the pathogenesis of glioma and its potential as a therapeutic target. By mediating cystine uptake and glutamate release, SLC7A11 promotes glutathione (GSH) synthesis, protecting glioma cells from oxidative stress-induced damage and maintaining the antioxidant defense mechanisms. Its expression levels are closely correlated with glioma malignancy and prognosis, with significantly elevated expression observed in high-grade gliomas, suggesting its involvement in malignant progression. Therapeutically, high SLC7A11 expression is associated with resistance to radiotherapy and chemotherapy, making it an attractive target. Studies have shown that inhibiting SLC7A11 function (e.g., using sulfasalazine) reduces GSH synthesis, induces reactive oxygen species (ROS) accumulation, and triggers ferroptosis in glioma cells. Furthermore, molecules such as p53, p62, and OTUB1 regulate SLC7A11 expression, influencing glioma development. Therapeutic strategies targeting SLC7A11, including the application of inhibitors and exploration of molecular targets, offer novel directions for glioma treatment.