Up-regulation of fibroblast growth factor-binding protein, by β-catenin during colon carcinogenesis

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...

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Published in:Cancer research (Chicago, Ill.) Vol. 63; no. 23; pp. 8085 - 8089
Main Authors: RAY, Ranjan, CABAL-MANZANO, Rafael, MOSER, Amy R, WALDMAN, Todd, ZIPPER, Laurie M, AIGNER, Achim, BYERS, Stephen W, RIEGEL, Anna T, WELLSTEIN, Anton
Format: Journal Article
Language:English
Published: Philadelphia, PA American Association for Cancer Research 01-12-2003
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Summary: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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content type line 23
ISSN:0008-5472
1538-7445