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Novel Detection and Differential Utilization of a c-myc Transcriptional Block in Colon Cancer Chemoprevention¹

Department of Oncology, Albert Einstein Cancer Center, Montefiore Medical Center, Bronx, New York 10467 [A. J. W., A. V., D. A., L. H. A.], and Department of Anatomical and Structural Biology, Albert Einstein College of Medicine, Bronx, New York 10461 [A. R. K., S. M. S., R. C. P., J. M. L., R. H. S.]

Mutations in the adenomatous polyposis coli (APC) gene, which initiate almost all human colon cancers, directly target the proto-oncogene, c-myc, by elevating ß-catenin/T-cell factor (TCF) signaling. We have shown that agents ascribed chemopreventive activity for colon cancer in fact also stimulate ß-catenin/TCF activity in vitro. Their effects on c-myc transcription were assayed using a novel variant of fluorescence in situ hybridization that detects c-myc transcription sites in intact nuclei. Increased transcriptional initiation of c-myc induced by the short-chain fatty acid, butyrate, consistent with elevated ß-catenin/TCF activity, was efficiently abrogated by a block to transcriptional elongation, resulting in decreased c-myc expression. 1,25-Dihydroxyvitamin D₃ also induced transcriptional blockage. In contrast, the nonsteroidal anti-inflammatory drug, sulindac, increased c-myc expression, an effect attributable at least in part to its failure to induce transcriptional blockage. We have described a novel approach for evaluating the effects of chemopreventive agents on the expression of a gene critical in colonic tumorigenesis.

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