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Cancer Cell. January 1, 2004; 5 (1): 91-102.

Small-molecule antagonists of the oncogenic Tcf/beta-catenin protein complex.

Lepourcelet M , Chen YN , France DS , Wang H , Crews P , Petersen F , Bruseo C , Wood AW , Shivdasani RA .

Key molecular lesions in colorectal and other cancers cause beta-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 beta-catenin, we screened libraries of natural compounds in a high-throughput assay for immunoenzymatic detection of the protein-protein interaction. Selected compounds disrupt Tcf/beta-catenin complexes in several independent in vitro assays and potently antagonize cellular effects of beta-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/beta-catenin complexes and define a general standard to establish mechanism-based activity of small molecule inhibitors of this pathogenic protein-protein interaction.

PubMed ID: 14749129
Article link: Cancer Cell.
Grant support: CA52955 NCI NIH HHS

Genes referenced: myc tcf4 tcf7l2

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