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Cdc42 and Rac1 are necessary for autotaxin‐induced tumor cell motility in A2058 melanoma cells
Author(s) -
Jung In Duk,
Lee Jangsoon,
Yun Seong Young,
Park Chang Gyo,
Choi Wahn Soo,
Lee Hyang Woo,
Choi Oksoon H,
Han Jeung Whan,
Lee Hoi Young
Publication year - 2002
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)03698-0
Subject(s) - autotaxin , rac1 , motility , cdc42 , focal adhesion , microbiology and biotechnology , angiogenesis , signal transduction , melanoma , cancer research , cell migration , lysophosphatidic acid , chemistry , biology , cell , biochemistry , receptor
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.