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Advances in Brief |
1 Lombardi Cancer Center, Georgetown University, Washington, DC, and
2 Department of Human Oncology, University of Wisconsin Medical School, Madison, Wisconsin
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 ß-catenin. In addition, FGF-BP expression is induced in dysplastic lesions in ApcMin/+ mice in parallel with the up-regulation of ß-catenin. Also, in cell culture studies FGF-BP is induced by ß-catenin through direct activation of the FGF-BP gene promoter. We conclude that FGF-BP is a target gene of ß-catenin.
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