The Role of Erastin in Ferroptosis and Its Prospects in Cancer Therapy

Yuechen Zhao,1 Yanqing Li,2 Ruifeng Zhang,1 Feng Wang,3 Tiejun Wang,1,* Yan Jiao4,* 1Department of Radiation Oncology, The Second Hospital of Jilin University, Changchun, People’s Republic of China; 2Department of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, People’s Republic of China; 3Department of Oral and Maxillofacial Surgery, Hospital of Stomatology, Jilin University, Changchun, People’s Republic of China; 4Department of Hepatobiliary and Pancreatic Surgery, The First Hospital of Jilin University, Changchun, People’s Republic of China*These authors contributed equally to this workCorrespondence: Tiejun WangDepartment of Radiation Oncology, The Second Hospital of Jilin University, No. 218 Ziqiang Street, Changchun 130022, People’s Republic of ChinaTel +8619904449098Email drwangtiejun@yeah.netYan JiaoDepartment of Hepatobiliary and Pancreatic Surgery, The First Hospital of Jilin University, No. 71 Xinmin Street, Changchun 130021, People’s Republic of ChinaTel +8613843101157Email lagelangri1@126.comAbstract: Erastin was initially discovered as a small molecule compound that selectively kills tumor cells expressing ST and RASV12 and was later widely investigated as an inducer of ferroptosis. Ferroptosis is a recently discovered form of cell death caused by peroxidation induced by the accumulation of intracellular lipid reactive oxygen species (L-ROS) in an iron-dependent manner. Erastin can mediate ferroptosis through a variety of molecules including the cystine-glutamate transport receptor (system XC−), the voltage-dependent anion channel (VDAC), and p53. Erastin is able to enhance the sensitivity of chemotherapy and radiotherapy, suggesting a promising future in cancer therapy. We hope that this review will help to better understand the role of erastin in ferroptosis and lay the foundation for further research and the development of erastin-based cancer therapies in the future.Keywords: erastin, ferroptosis, system XC−, p53, VDAC, cancer