Up-regulation of fibroblast growth factor-binding protein, by beta-catenin during colon carcinogenesis.
Up-regulation of fibroblast growth factor-binding protein, by beta-catenin during colon carcinogenesis.
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发表时间：
2003-12
期刊：
影响因子：
11.2
通讯作者：
R. Ray;R. Cabal-Manzano;A. Moser;T. Waldman;Laurie M. Zipper;A. Aigner;S. Byers;A. Riegel;A. Wellstein
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作者：
R. Ray;R. Cabal-Manzano;A. Moser;T. Waldman;Laurie M. Zipper;A. Aigner;S. Byers;A. Riegel;A. Wellstein
成纤维细胞生长因子结合蛋白（FGF-BP）从细胞外基质中释放固定化的fgf，并在癌症中作为血管生成开关分子发挥作用。在这里，我们发现FGF-BP在人类结肠早期发育不良病变中上调，这种病变通常与腺瘤性大肠息肉病的丧失和β -连环蛋白的上调有关。此外，在ApcMin/+小鼠的发育不良病变中，FGF-BP的表达与β -catenin的上调同时被诱导。此外，在细胞培养研究中，β -连环蛋白通过直接激活FGF-BP基因启动子诱导FGF-BP。我们认为FGF-BP是β -连环蛋白的靶基因。
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.