MUC1 drives epithelial-mesenchymal transition in renal carcinoma through Wnt/[beta]-catenin pathway and interaction withSNAILpromoter

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 indirectl...

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Bibliographic Details
Published in:Cancer letters 2014-05, Vol.346 (2), p.225
Main Authors: Gnemmi, Viviane, Bouillez, Audrey, Gaudelot, Kelly, Hémon, Brigitte, Ringot, Bélinda, Pottier, Nicolas, Glowacki, François, Villers, Arnauld, Vindrieux, David, Cauffiez, Christelle, Seuningen, Isabelle van, Bernard, David, Leroy, Xavier, Aubert, Sébastien, Perrais, Michaël
Format: Article
Language:English
Subjects:
Biopsy
Kidney cancer
Medical research
Metastasis
Peptides
Rodents
Transcription factors
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Summary: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.
ISSN:0304-3835
1872-7980
DOI:10.1016/j.canlet.2013.12.029