Fig. 6
Autophagy inhibition enhances the penfluridol-induced apoptotic effect in acute myeloid leukemia (AML) cells. a-c U937 and HL-60 cells were pretreated with 20 μM Z-VAD-fmk (a), chloroquine (CQ) (b), or 10 mM 3-methylamphetamine (3-MA) (c) for 1 h followed by penfluridol (7.5 μM) treatment for an additional 24 h. Levels of cleaved pro-poly (ADP ribose) polymerase (PARP), light chain (LC)3 conversion, and p62 degradation were detected by a Western blot analysis, and β-actin was used as a loading control. d and e U937, HL-60, and MV4–11 cells were pretreated with 20 μM CQ or 10 mM 3-MA for 1 h followed by 7.5 μM (d) or 5 μM (e) penfluridol treatment for an additional 24 h. The sub-G1 cell population was analyzed by flow cytometry following staining with propidium iodide (PI). Data are presented as the mean ± SD. ** p < 0.01; *** p < 0.001 versus the vehicle control group. # p < 0.05; ## p < 0.01 versus the penfluridol treatment only group