作者: Ki Young Jang , Soo-Jin Jeong , Sun-Hee Kim , Ji Hoon Jung , Ji-Hyun Kim
DOI: 10.1016/J.CANLET.2012.01.008
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摘要: Abstract We investigated the molecular mechanisms responsible for fisetin-induced apoptosis in U266 cells. Fisetin elicited cytotoxicity cells, manifested as an increased fraction of cells with sub-G1 content or stained positively TUNEL labeling. enhanced caspase-3 activation, downregulation Bcl-2 and Mcl-1L, upregulation Bax, Bim Bad. activated AMPK well its substrate acetyl-CoA carboxylase (ACC), along a decreased phosphorylation AKT mTOR. also stimulated generation ROS Conversely, compound C N-acetyl- l -cystein blocked apoptosis. Our data suggest that is through pathways.