Fig. 2
Penfluridol induces apoptosis of human acute myeloid leukemia (AML) cells with wild-type or mutant Fms-like tyrosine kinase 3 (FLT3). a HL-60 and U937 cells with wild-type FLT3 were treated with 7.5 μM penfluridol for 24 h, and nuclear fragmentation and condensation (arrows) as indicators of apoptosis were analyzed by fluorescence microscopy after DAPI staining, and the percentage of apoptotic cells was determined. Data are presented as the mean ± SD. *** p < 0.001 versus the control group. b HL-60 and U937 cells were treated with 7.5 μM penfluridol for 24 h and stained with propidium iodide (PI), then analyzed by flow cytometry. Percentages of cells at the G0/G1, S, G2/M, and sub-G1 phases were determined. Data are presented as the mean ± SD. * p < 0.05; ** p < 0.01 versus the control group. c and d HL-60 and U937 cells were treated with different concentrations of penfluridol for 24 h (c) or 7.5 μM penfluridol for different time points (d), and then the apoptosis-associated proteins, cleaved poly (ADP ribose) polymerase (PARP) and caspase-3, were detected by a Western blot analysis. β-actin served as a loading control. e and f Cell death in the sub-G1 phase (e) and cleaved PARP and caspase-3 proteins (f) were increased after penfluridol treatment with different concentrations and at different time points, in MV4–11 cells harboring mutant FLT3 (internal tandem duplication). Data are presented as the mean ± SD. *** p < 0.001 versus the control group