| Literature DB >> 24384091 |
Viviane Gnemmi1, Audrey Bouillez2, Kelly Gaudelot2, Brigitte Hémon2, Bélinda Ringot2, Nicolas Pottier3, François Glowacki4, Arnauld Villers5, David Vindrieux6, Christelle Cauffiez3, Isabelle Van Seuningen2, David Bernard6, Xavier Leroy7, Sébastien Aubert7, Michaël Perrais8.
Abstract
MUC1 is overexpressed in human carcinomas. The transcription factor SNAIL can activate epithelial-mesenchymal transition (EMT) in cancer cells. In this study, in renal carcinoma, we demonstrate that (i) MUC1 and SNAIL were overexpressed in human sarcomatoid carcinomas, (ii) SNAIL increased indirectly MUC1 expression, (iii) MUC1 overexpression induced EMT, (iv) MUC1 C-terminal domain (MUC1-C) and β-catenin increased SNAIL transcriptional activity by interaction with its promoter and (v) blocking MUC1-C nuclear localization decreased Wnt/β-catenin signaling pathway activation and SNAIL expression. Altogether, our findings demonstrate that MUC1 is an actor in EMT and appears as a new therapeutic target.Entities:
Keywords: Beta catenin; Epithelial mesenchymal transition; GO-203; MUC1; SNAIL
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Year: 2013 PMID： 24384091 DOI： 10.1016/j.canlet.2013.12.029
Source DB: PubMed Journal: Cancer Lett ISSN： 0304-3835 Impact factor: 8.679