Cancer Research Infection and Cancer: Biology, Therapeutics, and Prevention AACR Conference on Molecular Diagnostics - 2008
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[Cancer Research 64, 2534-2543, April 1, 2004]
© 2004 American Association for Cancer Research

Regular Articles

Stromal Cell-Derived Factor-1{alpha} Promotes Melanoma Cell Invasion across Basement Membranes Involving Stimulation of Membrane-Type 1 Matrix Metalloproteinase and Rho GTPase Activities

Rubén A. Bartolomé1, Beatriz G. Gálvez2, Natividad Longo3, Françoise Baleux4, Goos N. P. van Muijen5, Paloma Sánchez-Mateos3, Alicia G. Arroyo2 and Joaquin Teixidó1

1 Centro de Investigaciones Biológicas, Department of Immunology, Madrid, Spain; 2 Hospital Universitario de la Princesa, Department of Immunology, Madrid, Spain; 3 Servicio de Inmuno-Oncología, Hospital Universitario Gregorio Marañón, Madrid, Spain; 4 Institut Pasteur, Unité de Chimie Organique, Paris, France; 5 Department of Pathology, University Medical Centre, Nijmegen, the Netherlands

Tissue invasion by tumor cells involves their migration across basement membranes through activation of extracellular matrix degradation and cell motility mechanisms. Chemokines binding to their receptors provide chemotactic cues guiding cells to specific tissues and organs; they therefore could potentially participate in tumor cell dissemination. Melanoma cells express CXCR4, the receptor for the chemokine stromal cell-derived factor-1{alpha} (SDF-1{alpha}). Using Matrigel as a model, we show that SDF-1{alpha} promotes invasion of melanoma cells across basement membranes. Stimulation of membrane-type 1 matrix metalloproteinase (MT1-MMP) activity by SDF-1{alpha} was necessary for invasion, involving at least up-regulation in the expression of this metalloproteinase, as detected in the highly metastatic BLM melanoma cell line. Moreover, SDF-1{alpha} triggered the activation of the GTPases RhoA, Rac1, and Cdc42 on BLM cells, and expression of dominant-negative forms of RhoA and Rac1, but not Cdc42, substantially impaired the invasion of transfectants in response to SDF-1{alpha}, as well as the increase in MT1-MMP expression. Furthermore, CXCR4 expression on melanoma cells was notably augmented by transforming growth factor-ß1, a Matrigel component, whereas anti-transforming growth factor-ß antibodies inhibited increases in CXCR4 expression and melanoma cell invasion toward SDF-1{alpha}. The identification of SDF-1{alpha} as a potential stimulatory molecule for MT1-MMP as well as for RhoA and Rac1 activities during melanoma cell invasion, associated with an up-regulation in CXCR4 expression by interaction with basement membrane factors, could contribute to better knowledge of mechanisms stimulating melanoma cell dissemination.




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Copyright © 2004 by the American Association for Cancer Research.