HSP90B1-mediated plasma membrane localization of GLUT1 promotes radioresistance of glioblastomas

Ionizing radiation is a popular and effective treatment option for glioblastoma (GBM). However, resistance to radiation therapy inevitably occurs during treatment. It is urgent to investigate the mechanisms of radioresistance in GBM and to find ways to improve radiosensitivity. Here, we found that heat shock protein 90 beta family member 1 (HSP90B1) was significantly upregulated in radioresistant GBM cells. More importantly, HSP90B1 promoted the localization of glucose transporter type 1 (GLUT1) on plasma membrane, which in turn enhanced glycolytic activity and subsequently tumor growth and radioresistance of GBM cells. These findings imply that targeting HSP90B1 may effectively improve the efficacy of radiotherapy for GBM patients, bringing a new dawn to the treatment of glioblastoma.