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

2002/11/20 by In Duk Jung, Jangsoon Lee, Seong Young Yun +6 · 1 citation
Biochemistry, Genetics and Molecular Biology · #Sphingolipid Metabolism and Signaling #Microtubule and mitosis dynamics #Endoplasmic Reticulum Stress and Disease

paper · pdf · doi:10.1016/s0014-5793(02)03698-0

openalex publication_date 2002/11/20 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/05

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.

Citations

• Identification, purification, and partial sequence analysis of autotaxin, a novel motility-stimulating protein.
• Autotaxin Is an Exoenzyme Possessing 5′-Nucleotide Phosphodiesterase/ATP Pyrophosphatase and ATPase Activities
• Autotaxin has lysophospholipase D activity leading to tumor cell growth and motility by lysophosphatidic acid production

Cited by

• Autotaxin [wikipedia]