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  • Title: Lymphoid enhancer factor 1 makes cells resistant to transforming growth factor beta-induced repression of c-myc.
    Author: Sasaki T, Suzuki H, Yagi K, Furuhashi M, Yao R, Susa S, Noda T, Arai Y, Miyazono K, Kato M.
    Journal: Cancer Res; 2003 Feb 15; 63(4):801-6. PubMed ID: 12591729.
    Abstract:
    The activation of lymphoid enhancer factor (LEF)/T-cell factor (TCF)-mediated transcription by sustained expression of beta-catenin and the loss of transforming growth factor beta (TGF-beta) signaling are essential steps in carcinogenesis, particularly for cancers of the colon, breast, and liver. The oncogene c-myc is a common target of both of these signaling pathways and a key regulator of cell cycle progression. Here we have identified a novel LEF/TCF-responsive element in the promoter of the human c-myc gene. beta-Catenin activated the transcriptional activity of the c-myc promoter by binding to this element in various cell lines. When TCF-4 was bound to this element, TGF-beta dissociated beta-catenin and repressed the transcriptional activity of the c-myc promoter. However, TGF-beta could not dissociate beta-catenin and could not repress c-myc transcription when LEF-1 was bound to the element instead of TCF-4. These findings suggest that enhanced expression of LEF-1, which occurs frequently in colon cancer, may make cells refractory to the down-regulation of c-myc and the subsequent growth arrest induced by TGF-beta.
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