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 language | English (US) |
|---|---|
| Pages (from-to) | 351-356 |
| Number of pages | 6 |
| Journal | FEBS Letters |
| Volume | 532 |
| Issue number | 3 |
| DOIs | |
| State | Published - Dec 18 2002 |
| Externally published | Yes |
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Keywords
- Autotaxin
- Cdc42
- Focal adhesion kinase
- Rac1
ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Molecular Biology
Cite this
Cdc42 and Rac1 are necessary for autotaxin-induced tumor cell motility in A2058 melanoma cells. / 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.
In: FEBS Letters, Vol. 532, No. 3, 18.12.2002, p. 351-356.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Cdc42 and Rac1 are necessary for autotaxin-induced tumor cell motility in A2058 melanoma cells
AU - Jung, In Duk
AU - Lee, Jangsoon
AU - Yun, Seong Young
AU - Park, Chang Gyo
AU - Choi, Wahn Soo
AU - Lee, Hyang Woo
AU - Choi, Oksoon H.
AU - Han, Jeung Whan
AU - Lee, Hoi Young
PY - 2002/12/18
Y1 - 2002/12/18
N2 - 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.
AB - 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.
KW - Autotaxin
KW - Cdc42
KW - Focal adhesion kinase
KW - Rac1
UR - http://www.scopus.com/inward/record.url?scp=0037132539&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0037132539&partnerID=8YFLogxK
U2 - 10.1016/S0014-5793(02)03698-0
DO - 10.1016/S0014-5793(02)03698-0
M3 - Article
C2 - 12482591
AN - SCOPUS:0037132539
VL - 532
SP - 351
EP - 356
JO - FEBS Letters
JF - FEBS Letters
SN - 0014-5793
IS - 3
ER -