Cdc42 and Rac1 are necessary for autotaxin-induced tumor cell motility in A2058 melanoma cells

被引：28

作者：

Jung, ID

Lee, J

Yun, SY

Park, CG

Choi, WS

Lee, HW

Choi, OH

Han, JW

Lee, HY ^{[1
]}

机构：

[1] Konyang Univ, Coll Med, Nonsan 320711, South Korea

[2] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA

[3] Sungkyunkwan Univ, Coll Pharm, Suwon 440746, South Korea

[4] Meharry Med Coll, Dept Biochem, Nashville, TN 37208 USA

来源：

FEBS LETTERS | 2002年 / 532卷 / 03期

关键词：

autotaxin; Rac1; Cdc42; focal adhesion kinase;

D O I：

10.1016/S0014-5793(02)03698-0

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Autotaxin (ATX) is a strong motogen that can increase invasiveness and angiogenesis. In the present study, we investigated the signal transduction mechanism of ATX-induced tumor cell motility. Unlike N19RhoA expressing cells, the cells expressing N17Cdc42 or N17Rac1 showed reduced motility against ATX. ATX activated Cdc42 and Rac1 and increased complex formation between these small G proteins and p21-activated kinase (PAK). Furthermore, ATX phosphorylated focal adhesion kinase (FAK) that was not shown in cells expressing dominant negative mutants of Cdc42 or Rac1. Collectively, these data strongly indicate that Cdc42 and Rac1 are essential for ATX-induced tumor cell motility in A2058 melanoma cells, and that PAK and FAK might be also involved in the process. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

引用

页码：351 / 356

页数：6

共 40 条

[1] Vascular endothelial growth factor stimulates tyrosine phosphorylation and recruitment to new focal adhesions of focal adhesion kinase and paxillin in endothelial cells [J].