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Lepourcelet, Maina; Chen, Ying-Nan P.; France, Dennis S.; Wang, Huisheng; Crews, Phillip; Petersen, Frank; Bruseo, Charles; Wood, Alexander W.; Shivdasani, Ramesh A.
Cancer cell, 2004, 2004-Jan, 2004-01-00, 20040101, Letnik: 5, Številka: 1Journal Article
Key molecular lesions in colorectal and other cancers cause β-catenin-dependent transactivation of T cell factor (Tcf)-dependent genes. Disruption of this signal represents an opportunity for rational cancer therapy. To identify compounds that inhibit association between Tcf4 and β-catenin, we screened libraries of natural compounds in a high-throughput assay for immunoenzymatic detection of the protein-protein interaction. Selected compounds disrupt Tcf/β-catenin complexes in several independent in vitro assays and potently antagonize cellular effects of β-catenin-dependent activities, including reporter gene activation, c-myc or cyclin D1 expression, cell proliferation, and duplication of the Xenopus embryonic dorsal axis. These compounds thus meet predicted criteria for disrupting Tcf/β-catenin complexes and define a general standard to establish mechanism-based activity of small molecule inhibitors of this pathogenic protein-protein interaction.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Vir: Osebne bibliografije
in: SICRIS
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