The anticancer effects of trans-1,3-diphenyl-2,3-epoxypropan-1-one (DPEP), a
chalcone derivative, were investigated in human
leukemia HL-60 cells. Treatment of HL-60 cells with various concentration of DPEP resulted in a sequence of events characteristic of apoptosis, including loss of cell viability, morphological changes, and increased sub-G1
DNA content. We demonstrated that DPEP elevates
reactive oxygen species (ROS) levels in HL-60 cells, and that the ROS scavenger
N-acetylcysteine (NAC) could block DPEP-induced ROS generation and apoptosis. Western blot analysis revealed that DPEP inhibits Bcl-xL expression, leading to
caspase-3 activation and
poly-ADP-ribose polymerase (PARP) cleavage, thereby inducing apoptosis. However, NAC pre-treatment significantly inhibited the activation of
caspase-3 and PARP cleavage and reduced Bcl-xL levels. These findings provide the first evidence that DPEP may inhibit the growth of HL-60 cells and induce apoptosis through a ROS-mediated Bcl-xL pathway.