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

doi:10.1016/S0014-5793(02)03698-0

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

School of Medicine

Research output: Contribution to journal › Article › peer-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 language	English (US)
Pages (from-to)	351-356
Number of pages	6
Journal	FEBS Letters
Volume	532
Issue number	3
DOIs	https://doi.org/10.1016/S0014-5793(02)03698-0
State	Published - Dec 18 2002

Keywords

Autotaxin
Cdc42
Focal adhesion kinase
Rac1

ASJC Scopus subject areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

Access to Document

10.1016/S0014-5793(02)03698-0

Fingerprint Dive into the research topics of 'Cdc42 and Rac1 are necessary for autotaxin-induced tumor cell motility in A2058 melanoma cells'. Together they form a unique fingerprint.

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 › peer-review

@article{c8fa663a59f04a159f2f998fe12c4748,

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

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.",

keywords = "Autotaxin, Cdc42, Focal adhesion kinase, Rac1",

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

note = "Funding Information: This work was supported by a Korea Research Foundation Grant (KRF-2001-002-F00088). We would like to thank Dr. Seung-Kil Park for N19RhoA, and Dr. Dongeun Park for GST-PBD.",

year = "2002",

month = dec,

day = "18",

doi = "10.1016/S0014-5793(02)03698-0",

language = "English (US)",

volume = "532",

pages = "351--356",

journal = "FEBS Letters",

issn = "0014-5793",

publisher = "Elsevier",

number = "3",

}

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

N1 - Funding Information: This work was supported by a Korea Research Foundation Grant (KRF-2001-002-F00088). We would like to thank Dr. Seung-Kil Park for N19RhoA, and Dr. Dongeun Park for GST-PBD.

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 -