CAS/Crk Coupling Serves as a "Molecular Switch" for Induction of Cell Migration

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© The Rockefeller University Press, 0021-9525/1998//961 $5.00
The Journal of Cell Biology, Volume 140, Number 4, , 1998 961-972

Article

CAS/Crk Coupling Serves as a "Molecular Switch" for Induction of Cell Migration

Richard L. Klemke^*, Jie Leng^*, Rachel Molander^*, Peter C. Brooks^*, Kristiina Vuori, and David A. Cheresh^*

^* Departments of Immunology and Vascular Biology, The Scripps Research Institute, La Jolla, California 92037; The La Jolla Cancer Research Center, The Burnham Institute, La Jolla, California 92037

Abstract. Carcinoma cells selected for their ability to migratein vitro showed enhanced invasive properties in vivo. Associatedwith this induction of migration was the anchorage-dependentphosphorylation of p130CAS (Crk-associated substrate), leadingto its coupling to the adaptor protein c-CrkII (Crk). In fact,expression of CAS or its adaptor protein partner Crk was sufficient to promote cell migration, and this depended on CAS tyrosinephosphorylation facilitating an SH2-mediated complex with Crk.Cytokine-stimulated cell migration was blocked by CAS lackingthe Crk binding site or Crk containing a mutant SH2 domain.This migration response was characterized by CAS/Crk localizationto membrane ruffles and blocked by the dominant-negative GTPase,Rac, but not Ras. Thus, CAS/Crk assembly serves as a "molecularswitch" for the induction of cell migration and appears tocontribute to the invasive property of tumors.

1. Abbreviations used in this paper: aa, amino acid(s); CAS,Crk-associated substrate; ECM, extracellular matrix; FAK, focaladhesion kinase; FBM, fibroblast basal medium; IGF-1, insulin-likegrowth factor 1; SH, src homology.

The authors would like to thank Drs. A. Minden and M. Karin(University of California, San Diego, CA) for providing Racand Ras constructs. We are also grateful to Dr. M. Matsuda(International Medical Center of Japan, Tokyo, Japan) for originalCrk constructs, and Drs. H. Hirai (University of Tokyo, Tokyo,Japan) and B. Mayer (Howard Hughes Medical Institute, The Children'sHospital, Boston, MA) for CAS cDNA constructs and expressionvectors.

D.A. Cheresh was supported by grants HL-54444, CA-50286, andCA-45726 from the National Institutes of Health (NIH). R.L.Klemke was supported by a fellowship award from the JosephDrown Foundation. J. Leng was supported by the U.S. Army MedicalResearch and Material Command under DAMD17-96-1-6104. K. Vuoriwas supported by grant CA-71560 from the NIH. K. Vuori is aPEW scholar in Biomedical Sciences. This manuscript is number11052-IMM from The Scripps Research Institute.

Address all correspondence to Richard L. Klemke, Departmentsof Immunology and Vascular Biology, IMM-24, The Scripps ResearchInstitute, 10550 N. Torrey Pines Rd., La Jolla, CA 92037. Tel.:(619) 784-8164. Fax: 619-784-8926. E-mail: klemke{at}scripps.edu

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Kwong, L., Wozniak, M. A., Collins, A. S., Wilson, S. D., Keely, P. J. (2003). R-Ras Promotes Focal Adhesion Formation through Focal Adhesion Kinase and p130Cas by a Novel Mechanism That Differs from Integrins. Mol. Cell. Biol. 23: 933-949 [Abstract] [Full Text]
Cai, D., Felekkis, K. N., Near, R. I., O'Neill, G. M., van Seventer, J. M., Golemis, E. A., Lerner, A. (2003). The GDP Exchange Factor AND-34 Is Expressed in B Cells, Associates With HEF1, and Activates Cdc42. J. Immunol. 170: 969-978 [Abstract] [Full Text]
Yigzaw, Y., Poppleton, H. M., Sreejayan, N., Hassid, A., Patel, T. B. (2003). Protein-tyrosine Phosphatase-1B (PTP1B) Mediates the Anti-migratory Actions of Sprouty. J. Biol. Chem. 278: 284-288 [Abstract] [Full Text]
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Hinsby, A. M., Olsen, J. V., Bennett, K. L., Mann, M. (2003). Signaling Initiated by Overexpression of the Fibroblast Growth Factor Receptor-1 Investigated by Mass Spectrometry. Mol. Cell. Proteomics 2: 29-36 [Abstract] [Full Text]
Lerman, O. Z., Galiano, R. D., Armour, M., Levine, J. P., Gurtner, G. C. (2003). Cellular Dysfunction in the Diabetic Fibroblast: Impairment in Migration, Vascular Endothelial Growth Factor Production, and Response to Hypoxia. Am. J. Pathol. 162: 303-312 [Abstract] [Full Text]
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