14-3-3epsilon inhibits MK5-mediated cell migration by disrupting F-actin polymerization

被引：58
作者：
Tak, Heejae
Jang, Eunsun
Kim, Seung Beom
Park, Jinhwi
Suk, Jinkyu
Yoon, Yoo Sik
Ahn, Jeong Keun
Lee, Jeung-Hoon
Joe, Cheol O. [1 ]
机构：
[1] Korea Adv Inst Sci & Technol, Dept Biol Sci, Taejon 305701, South Korea
[2] Chung Ang Univ, Coll Med, Seoul 156756, South Korea
[3] Chungnam Natl Univ, Dept Microbiol, Taejon 305764, South Korea
[4] Chungnam Natl Univ, Sch Med, Dept Dermatol, Taejon 301040, South Korea
来源：
CELLULAR SIGNALLING | 2007年 / 19卷 / 11期
基金：
新加坡国家研究基金会;
关键词：
MAPK; MK5; 14-3-3; epsilon; HSP27; actin polymerization; cell migration; TNF alpha;
D O I：
10.1016/j.cellsig.2007.07.016
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
The signal pathway by which 14-3-3 epsilon inhibits cell migration induced by MAPK-activated protein kinase 5 (MK5) was investigated in cultured HeLa cells. Both in vivo and in vitro analyses have revealed that 14-3-3e interacts with MK5. 14-3-3e bound to MK5 inhibits the pbosphorylation of HSP27, a known substrate of MK5. Disturbance of actin cytoskeleton organization by 14-3-3 epsilon was shown in transfected cells transiently expressing 14-3-3 epsilon as well as established cells stably expressing 14-3-3e. Moreover, overexpression of 14-3-3e resulted in the inhibition of cell migration induced by MK5 overexpression or TNF alpha treatment. Our results suggest that 14-3-3 epsilon bound to MK5 inhibits cell migration by inhibiting the phosphorylation of HSP27 whose phospborylation regulates F-actin polymerization, actin cytoskeleton organization and subsequent actinfilament dynamics. (C) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码：2379 / 2387
页数：9
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