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

In Duk Jung, Jangsoon Lee, Seong Young Yun, Chang Gyo Park, Wahn Soo Choi, Hyang Woo Lee, Oksoon H. Choi, Jeung Whan Han, Hoi Young Lee

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish (US)
Pages (from-to)351-356
Number of pages6
JournalFEBS Letters
Volume532
Issue number3
DOIs
StatePublished - Dec 18 2002

Keywords

  • Autotaxin
  • Cdc42
  • Focal adhesion kinase
  • Rac1

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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