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Activation of reactive oxygen species/AMP activated protein kinase signaling mediates fisetin-induced apoptosis in multiple myeloma U266 cells.

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-1(L), 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.

journal_name

Cancer Lett

journal_title

Cancer letters

authors

Jang KY,Jeong SJ,Kim SH,Jung JH,Kim JH,Koh W,Chen CY,Kim SH

doi

10.1016/j.canlet.2012.01.008

subject

Has Abstract

pub_date

2012-06-28 00:00:00

pages

197-202

issue

2

eissn

0304-3835

issn

1872-7980

pii

S0304-3835(12)00033-X

journal_volume

319

pub_type

杂志文章

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