Fig. 2
TREM2 inhibition remarkably enhanced the radiosensitivity of GBM through interfering with DNA damage repair pathway. (A) The infected efficiencies of EGFP-labeled lentivirus expressing TREM2-shRNA and NC-shRNA in GBM cells were observed under fluorescence microscope (scale bar: 100 μm); (B) The expression of TREM2 in GBM cells after TREM2 knockdown were detected by western blot; (C)-(E) The colony formation of GBM-NC cells and GBMTREM2−KD cells treated with radiotherapy at different doses, and the survival curves were fitted based on signal-hit multitarget model and linear-quadratic model, respectively, data are presented as mean ± SD, n = 3; (F) The expression of apoptotic marker PARP1 and cleaved PARP1, DNA damage marker γ-H2AX in GBM-NC and GBMTREM2−KD cells 24 h after exposing to radiotherapy (2 Gy) were detected by western blot; (G) The expression of TREM2 in GBM cells 48 h after TREM2 silencing with different siTREM2s were detected by western blot; (H) The expression of DNA-PKcs, KU70 and KU80 in GBM cells 48 h after TREM2 silencing were detected by western blot