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• W1993334239 abstract "We investigated the molecular mechanisms responsible for fisetin-induced apoptosis in U266 cells. Fisetin elicited the cytotoxicity in U266 cells, manifested as an increased fraction of the cells with sub-G1 content or stained positively with TUNEL labeling. Fisetin enhanced caspase-3 activation, downregulation of Bcl-2 and Mcl-1L, and upregulation of Bax, Bim and Bad. Fisetin activated AMPK as well as its substrate acetyl-CoA carboxylase (ACC), along with a decreased phosphorylation of AKT and mTOR. Fisetin also stimulated generation of ROS in U266 cells. Conversely, compound C or N-acetyl-l-cystein blocked fisetin-induced apoptosis. Our data suggest that fisetin-induced apoptosis in U266 cells is through ROS and AMPK pathways." @default.
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• W1993334239 date "2012-06-01" @default.
• W1993334239 modified "2023-09-23" @default.
• W1993334239 title "Activation of reactive oxygen species/AMP activated protein kinase signaling mediates fisetin-induced apoptosis in multiple myeloma U266 cells" @default.
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• W1993334239 doi "https://doi.org/10.1016/j.canlet.2012.01.008" @default.
• W1993334239 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22261340" @default.
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