作者: P. MILLET , C. GRANOTIER , O. ETIENNE , F.D. BOUSSIN
关键词: Telomerase 、 PI3K/AKT/mTOR pathway 、 DNA repair 、 Cancer research 、 Biology 、 Telomerase reverse transcriptase 、 Cell cycle 、 Molecular biology 、 Telomere 、 Glioma 、 Cancer cell
摘要: Tumor relapse after radiotherapy is a great concern in the treatment of high-grade gliomas. Inhibition PI3-kinase/AKT pathway known to radiosensitize cancer cells and delay their DNA repair irradiation. In this study, we show that radiosensitization CB193 T98G, two glioma cell lines, by PI3K inhibitor LY294002, correlates with induction G1 G2/M arrest, but inconsistently linked delayed double-strand break (DSBs) repair. The PI3K/AKT has been shown activate radioprotective factors such as telomerase, whose inhibition may contribute cells. However, radiation upregulates telomerase activity LY-294002-treated well untreated controls, demonstrating PI3K/AKT-independent activation. Our study suggests radiosensitizing strategies based on PI3-kinase gliomas be optimized additional treatments targeting either or telomere maintenance.