Abstract
Accumulating evidence indicates that CDK2 promotes hyperproliferation and is associated to poor prognosis in multiple cancer cells. However, the physiological role of CDK2 in GBM and the biological mechanism still remains unclear. In this study, we identified that CDK2 expression was significantly enriched in GBM tumors compared with normal brain. Additionally, CDK2 was functionally required for tumor proliferation and its expression was associated to poor prognosis in GBM patients. Mechanically, CDK2 induced radio resistance in GBM cells and CDK2 knock down increased cell apoptosis when combined with radiotherapy. Therapeutically, we found that CDK2 inhibitor attenuated tumor growth both in vitro and in vivo. Collectively, CDK2 promotes proliferation, induces radio resistance in GBM, and could become a therapeutic target for GBM.