Author/Authors :
Marco Gnemmi، نويسنده , , Viviane and Bouillez، نويسنده , , Audrey and Gaudelot، نويسنده , , Kelly and Hémon، نويسنده , , Brigitte and Ringot، نويسنده , , Bélinda and Pottier، نويسنده , , Nicolas and Glowacki، نويسنده , , François and Villers، نويسنده , , Arnauld and Vindrieux، نويسنده , , David and Cauffiez، نويسنده , , Christelle and Seuningen، نويسنده , , Isabelle Van and Bernard، نويسنده , , David and Leroy، نويسنده , , Xavier L. Aubert، نويسنده , , Sébastien and Perrais، نويسنده , , Michaël، نويسنده ,
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.
Keywords :
Beta catenin , GO-203 , Snail , MUC1 , Epithelial mesenchymal transition
