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Papers In Press, published online ahead of print March 7, 2007
J. Biol. Chem, 10.1074/jbc.M611739200
Submitted on December 21, 2006
Accepted on March 7, 2007

Shedding of syndecan-1 by stromal fibroblasts stimulates human breast cancer cell proliferation via FGF2 activation

Gui Su, Stacy A. Blaine, Dianhua Qiao, and Andreas Friedl

Pathology and Laboratory Medicine, University of Wisconsin-Madison, Madison, WI 53792-8550

Corresponding Author: afriedl{at}wisc.edu

The cell surface heparan sulfate proteoglycan syndecan-1 is induced in stromal fibroblasts of breast carcinomas and participates in a reciprocal feedback loop which stimulates carcinoma cell growth in vitro and in vivo. To define the molecular mechanism of carcinoma growth stimulation, a three-dimensional co-culture model was developed which combines T47D breast carcinoma cells with immortalized human mammary fibroblasts in collagen gels. By silencing endogenous syndecan-1 induction with siRNA and expressing mutant murine syndecan-1 constructs, it was determined that carcinoma cell mitogenesis required proteolytic shedding of syndecan-1 from the fibroblast surface. The paracrine growth signal was mediated by the syndecan-1 heparan sulfate chains rather than the ectodomain of the core protein and required fibroblast growth factor 2 and stroma-derived factor 1. This paracrine pathway may provide an opportunity for the therapeutic disruption of stroma-epithelial signaling.


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[Abstract] [Full Text] [PDF]


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