Research Paper Volume 9, Issue 4 pp 1233—1247

Figure 5. GLI1 acted as an effector inducing non-canonical TMZ-resistance in glioma cells. (A) Relative expression of GLI1 in U87, U87 OE and U87 KD. (B) Effect of GLI1 on cell proliferation was evaluated by CCK8 assays in U87, U87 OE and U87 KD cells. (C) Western blot analysis showed GLI1, γH2AX, p-ATM and ATM proteins expression in U87 and U87 OE treated with GANT61 (5 μM) for 48 h. β-actin was used as an internal control. (D) U87, U87 OE and U87 KD were examined for their sensitivity to TMZ at concentration of 100 µM. (E) Western blot analysis showed γH2AX, p-ATM and ATM proteins expression in U87, U87 OE and U87 KD treated with TMZ. β-actin was used as an internal control. Data are shown as mean±SEM for the three replicates. Statistical significance levels are indicated as: *P < 0.05; **P < 0.01 and ***P < 0.001.