文献类型：期刊文献

英文题名：Progress in research on the mechanisms and therapeutic strategies of SLC7A11 regulation in glioma

作者：Wei, Qianfeng[1];Xiong, Bangfa[1];Yang, Guangming[1];Wang, Jiahui[1];Chai, Erqing[1,2]

第一作者：Wei, Qianfeng

通信作者：Chai, EQ[1];Chai, EQ[2]

机构：[1]Gansu Univ Chinese Med, Sch Clin Med 1, Lanzhuo 730099, Peoples R China;[2]Gansu Prov Hosp, Cerebrovasc Dis Ctr, Key Lab Cerebrovasc, Dis Gansu Prov, Lanzhuo 730099, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Sch Clin Med 1, Lanzhuo 730099, Peoples R China;[2]corresponding author), Gansu Prov Hosp, Cerebrovasc Dis Ctr, Key Lab Cerebrovasc, Dis Gansu Prov, Lanzhuo 730099, Peoples R China.|[10735]甘肃中医药大学;

年份：2025

卷号：17

期号：1

外文期刊名：DISCOVER ONCOLOGY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001655343900011)】；

基金：This study was supported by the Gansu Province Science and Technology Innovation Platform Project (23GSSYB-8, 2244YFA030), the Gansu Province Natural Science Foundation Project (23JRRA1278), and the Gansu Provincial People's Hospital Science and Technology Innovation Platform Fund Project (21GSSYB-11, 24GSSYD-10).

语种：英文

外文关键词：Glioma; Ferroptosis; GSH

摘要：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.