Ray Ranjan, Cabal-Manzano Rafael, Moser Amy R, Waldman Todd, Zipper Laurie M, Aigner Achim, Byers Stephen W, Riegel Anna T, Wellstein Anton
Lombardi Cancer Center, Georgetown University, Washington, DC 20057, USA.
Cancer Res. 2003 Dec 1;63(23):8085-9.
Fibroblast growth factor-binding protein (FGF-BP) releases immobilized FGFs from the extracellular matrix and can function as an angiogenic switch molecule in cancer. Here we show that FGF-BP is up-regulated in early dysplastic lesions of the human colon that are typically associated with a loss of adenomatous polyposis coli and up-regulation of beta-catenin. In addition, FGF-BP expression is induced in dysplastic lesions in ApcMin/+ mice in parallel with the up-regulation of beta-catenin. Also, in cell culture studies FGF-BP is induced by beta-catenin through direct activation of the FGF-BP gene promoter. We conclude that FGF-BP is a target gene of beta-catenin.
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