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Published 11 October 2004. doi:10.1083/jcb.200404171
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 167, Number 1, 171-181
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Article

The syndecan-1 ectodomain regulates {alpha}vß3 integrin activity in human mammary carcinoma cells



DeannaLee M. Beauvais, Brandon J. Burbach, and Alan C. Rapraeger

Department of Pathology and Laboratory Medicine and Program in Molecular and Cellular Pharmacology, University of Wisconsin-Madison, Madison, WI 53706

Correspondence to Alan C. Rapraeger: acraprae{at}wisc.edu

The {alpha}vß3 integrin participates in cell morphogenesis, growth factor signaling, and cell survival. Activation of the integrin is central to these processes and is influenced by specific ECM components, which engage both integrins and syndecans. This paper demonstrates that the {alpha}vß3 integrin and syndecan-1 (S1) are functionally coupled. The integrin is dependent on the syndecan to become activated and to mediate signals required for MDA-MB-231 and MDA-MB-435 human mammary carcinoma cell spreading on vitronectin or S1-specific antibody. Coupling of the syndecan to {alpha}vß3 requires the S1 ectodomain (ED), as ectopic expression of glycosylphosphatidylinositol-linked S1ED enhances {alpha}vß3 recognition of vitronectin; and treatments that target this domain, including competition with recombinant S1ED protein or anti-S1ED antibodies, mutation of the S1ED, or down-regulation of S1 expression by small-interfering RNAs, disrupt {alpha}vß3-dependent cell spreading and migration. Thus, S1 is likely to be a critical regulator of many cellular behaviors that depend on activated {alpha}vß3 integrins.

Abbreviations used in this paper: COL, collagen; ED, ectodomain; FN, fibronectin; GPI, glycosylphosphatidylinositol; Hb, Hepes-buffered; HS, heparan sulfate; hS1, human S1; IMD, integrin-mediated death; LN, laminin; mS1, mouse S1; pAb, polyclonal antibody; S1, syndecan-1; siRNA, small-interfering RNA; TM, transmembrane; VN, vitronectin.


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