AMP-activated protein kinase is required for induction of apoptosis and epithelial-to-mesenchymal transition

被引：29
|
作者：
Wang, Xunde [1 ]
Pan, Xinchao [1 ]
Song, Jianguo [1 ]
机构：
[1] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, Mol Cell Biol Lab, Shanghai 200031, Peoples R China
来源：
CELLULAR SIGNALLING | 2010年 / 22卷 / 11期
关键词：
AMP-activated protein kinase; TGF-beta; Epithelial-to-mesenchymal transition; Apoptosis; GROWTH-FACTOR-BETA; FATTY-ACID OXIDATION; TGF-BETA; TUMOR SUPPRESSION; LIVER; FIBROSIS; METABOLISM; UPSTREAM; PATHWAY; CELLS;
D O I：
10.1016/j.cellsig.2010.07.008
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
AMP-activated protein kinase (AMPK) is a serine/threonine protein kinase which has been implicated in the regulation of cellular energy homeostasis. Relatively very little is known about its role in other cellular processes. We observed that AMPK-alpha can be activated by transforming growth factor-beta 1 (TGF-beta 1) in mouse hepatocytes. Inhibition of AMPK by Compound C, a selective AMPK-alpha inhibitor, inhibited TGF-beta 1-induced apoptosis and EMT in hepatocytes. In addition, overexpression of a dominant-negative form of AMPK-alpha subunit also suppressed TGF-beta 1-induced EMT and apoptosis in AML12 cells. Furthermore, inhibition of AMPK suppressed TGF-beta 1-induced Smad3 transcriptional activity. This study indicates that AMPK is able to modulate Smad3 transcriptional activity, which plays an important role in TGF-beta 1-induced apoptosis and EMT. (C) 2010 Elsevier Inc. All rights reserved.
引用
收藏
页码：1790 / 1797
页数：8
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