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[Cancer Research 63, 1192-1197, March 15, 2003]
© 2003 American Association for Cancer Research

Advances in Brief

A Nodal- and ALK4-independent Signaling Pathway Activated by Cripto-1 through Glypican-1 and c-Src1

Caterina Bianco, Luigi Strizzi, Aasia Rehman, Nicola Normanno, Christian Wechselberger, Youping Sun, Nadia Khan, Morihisa Hirota, Heather Adkins, Kevin Williams, Richard U. Margolis, Michele Sanicola and David S. Salomon2

Mammary Biology and Tumorigenesis Laboratory, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 [C. B., L. S., A. R., Y. S., N. K., M. H., D. S. S.]; Experimental Oncology B Unit, Istituto Fondazione Pascale, Naples 80131, Italy [N. N.]; Upper Austrian Research GmbH Zentrum, Linz 4020, Austria [C. W.]; Biogen, Inc., Cambridge, Massachusetts 02142 [H. A., K. W., M. S.]; and Department of Pharmacology, New York University Medical Center, New York, New York 10016 [R. U. M.]

Human Cripto-1 (CR-1) is a member of the epidermal growth factor-Cripto FRL1 Cryptic family that has been shown to function as a coreceptor with the type I Activin serine-threonine kinase receptor ALK4 for the transforming growth factor ß-related peptide Nodal. However, CR-1 can also activate the mitogen-activated protein kinase and Akt pathways independently of Nodal and ALK4 by an unknown mechanism. Here, we demonstrate that CR-1 specifically binds to Glypican-1, a membrane-associated heparan sulfate proteoglycan, and activates the tyrosine kinase c-Src, triggering the mitogen-activated protein kinase and Akt signaling pathways. Finally, an active Src kinase is necessary for CR-1 to induce in vitro transformation and migration in mouse mammary epithelial cells.




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