Ko, Eun-YiLee, Seung-HongKo, Ji-YeonMoon, Jeong YongYoon, Weon-JongAhn, GinnaeRoh, Seong WoonCho, KichulJeon, You-JinKim, DaekyungKim, Kil-Nam2016-06-032016-06-032015-08-031611-2156http://hdl.handle.net/2003/3502510.17877/DE290R-17073The 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 pretreatment 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.enEXCLI Journal;Vol. 14, 2015http://creativecommons.org/licenses/by/4.0/anticancertrans-1,3-diphenyl-2,3-epoxypropan-1-one (DPEP)apoptosisreactive oxygen species (ROS)Bcl-xL61010.17179/excli2015-373article (journal)