Fig. 4

Radotinib/Ara-C induces caspase-dependent apoptosis and activates caspase-3 activity in HL60 and HEL92.1.7 cells. The cells were also collected and treated under the same conditions described in Fig. 2. a Caspase-3 activity induced by radotinib and Ara-C stimulation in HL60 cells. b Caspase-3 activity induced by radotinib and Ara-C stimulation in HEL92.1.7 cells. c-e The expression of cleaved caspase-3, cleaved caspase-7, and cleaved caspase-9 was analyzed by SDS-PAGE, followed by western blotting using specific antibodies. f HL60 cells were incubated with 5 μM radotinib and 50 nM Ara-C in the presence or absence of Z-VAD-FMK (10 μM) for 48 h and then harvested. Cells were analyzed by capase-3 activity. g HL60 cells were also collected and treated under the same conditions described in Fig. 4f. Cells were analyzed by immunoblotting using an anti-cPARP-1 mAb and an anti-cleaved caspase-3 mAb. h HL60 cells were also collected and treated under the same conditions described in Fig. 3e. Cells were analyzed by immunoblotting using an anti-cPARP-1 mAb and an anti-cleaved caspase-3 mAb. The experiments were repeated three times and the data show representative results. The membrane was stripped and re-probed with an anti-β-actin mAb to confirm equal loading. These data represent the means ± SEM. Significantly different from control (*) or combination of radotinib and Ara-C (#); ***, ###: P < 0.001. R, radotinib; A, Ara-C; R + A, combination of radotinib and Ara-C; BA, bongkrekic acid