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

FEBS Letters

Yun, Seong Young²  Park, Chang Gyo²  Choi, Wahn Soo⁴  Jung, In Duk²  Lee, Hyang Woo³  Lee, Jangsoon²  Lee, Hoi Young²  Choi, Oksoon H¹  Han, Jeung Whan³ 

[1] Department of Biochemistry, Meharry Medical College, Nashville, TN 37208, USA;College of Medicine, Konyang University, Nonsan 320-711, South Korea;College of Pharmacy, Sungkyunkwan University, Suwon 440-746, South Korea;Laboratory of Molecular Immunology, NHLBI, National Institutes of Health, Bethesda, MD 20892-1760, USA

关键词: Autotaxin;    Rac1;    Cdc42;    Focal adhesion kinase;    ATX;    autotaxin;    PI3K;    phosphatidylinositide 3-kinase;    lysoPLD;    lysophospholipase D;    LPA;    lysophosphatidic acid;    FAK;    focal adhesion kinase;    PAK;    p21-activated kinase;    NPP;    nucleotide-pyrophosphatase phosphodiesterase;    PTx;    pertussis toxin;   

DOI  :  10.1016/S0014-5793(02)03698-0

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 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.

【 授权许可】

Unknown