1. Cdc42 and Rac1 are necessary for autotaxin-induced tumor cell motility in A2058 melanoma cells
- Author
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Seong Young Yun, Hyang Woo Lee, Oksoon Hong Choi, Hoi Young Lee, Jeung Whan Han, Jangsoon Lee, Wahn Soo Choi, Chang Gyo Park, and In Duk Jung
- Subjects
rac1 GTP-Binding Protein ,Angiogenesis ,Immunoblotting ,Biophysics ,Motility ,RAC1 ,CDC42 ,macromolecular substances ,Biology ,Transfection ,Biochemistry ,Focal adhesion ,Structural Biology ,Cell Movement ,GTP-Binding Proteins ,Multienzyme Complexes ,Genetics ,Tumor Cells, Cultured ,Humans ,Cdc42 ,Phosphorylation ,Pyrophosphatases ,cdc42 GTP-Binding Protein ,Molecular Biology ,Melanoma ,Cells, Cultured ,Genes, Dominant ,Glycoproteins ,Dose-Response Relationship, Drug ,Kinase ,Phosphoric Diester Hydrolases ,Focal adhesion kinase ,Glucose-6-Phosphate Isomerase ,Cell Biology ,Protein-Tyrosine Kinases ,Precipitin Tests ,Recombinant Proteins ,Autotaxin ,Pertussis Toxin ,Phosphodiesterase I ,Focal Adhesion Kinase 1 ,Focal Adhesion Protein-Tyrosine Kinases ,Mutation ,Cancer research ,Signal transduction ,biological phenomena, cell phenomena, and immunity ,Rac1 ,Plasmids - 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.
- Published
- 2002