Up-Regulation Of Fibroblast Growth Factor-Binding Protein, By Beta-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 upregulated 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.