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A SNAIL1–SMAD3/4 transcriptional repressor complex promotes TGF‑β mediated epithelial–mesenchymal transition

Vincent, Theresa (author)
Karolinska Institutet
Neve, Etienne P. A. (author)
Karolinska Institutet
Johnson, Jill R. (author)
Department of Cell and Molecular Biology, Karolinska Institute, 17177 Stockholm, Sweden
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Kukalev, Alexander (author)
Department of Cell and Molecular Biology, Karolinska Institute, 17177 Stockholm, Sweden
Rojo, Federico (author)
Oncology Department, Programa de Recerca en Càncer, IMIM-Hospital del Mar, 08003 Barcelona, Spain
Albanell, Joan (author)
Oncology Department, Programa de Recerca en Càncer, IMIM-Hospital del Mar, 08003 Barcelona, Spain
Pietras, Kristian (author)
Karolinska Institutet
Virtanen, Ismo (author)
Institute of Biomedicine/Anatomy, FI‑00014, University of Helsinki, Finland
Philipson, Lennart (author)
Karolinska Institutet
Leopold, Philip L. (author)
Department of Chemistry, Chemical Biology, and Biomedical Engineering, Stevens Institute of Technology, New Jersey 07030, USA
Crystal, Ronald G. (author)
Department of Genetic Medicine, Weill Medical College of Cornell University, New York 10065, USA
de Herreros, Antonio Garcia (author)
Oncology Department, Programa de Recerca en Càncer, IMIM-Hospital del Mar, 08003 Barcelona, Spain
Moustakas, Aristidis (author)
Uppsala universitet,Ludwiginstitutet för cancerforskning
Pettersson, Ralf F. (author)
Ludwig Institute for Cancer Research, Stockholm Branch, 17177 Stockholm, Sweden
Fuxe, Jonas (author)
Karolinska Institutet
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 (creator_code:org_t)
2009-07-13
2009
English.
In: Nature Cell Biology. - : Springer Science and Business Media LLC. - 1465-7392 .- 1476-4679. ; 11:8, s. 943-950
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  • Journal article (peer-reviewed)
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  • Epithelial-mesenchymal transition (EMT) is essential for organogenesis and is triggered during carcinoma progression to an invasive state. Transforming growth factor-β (TGF-β) cooperates with signalling pathways, such as Ras and Wnt, to induce EMT, but the molecular mechanisms are not clear. Here, we report that SMAD3 and SMAD4 interact and form a complex with SNAIL1, a transcriptional repressor and promoter of EMT. The SNAIL1-SMAD3/4 complex was targeted to the gene promoters of CAR, a tight-junction protein, and E-cadherin during TGF-β-driven EMT in breast epithelial cells. SNAIL1 and SMAD3/4 acted as co-repressors of CAR, occludin, claudin-3 and E-cadherin promoters in transfected cells. Conversely, co-silencing of SNAIL1 and SMAD4 by siRNA inhibited repression of CAR and occludin during EMT. Moreover, loss of CAR and E-cadherin correlated with nuclear co-expression of SNAIL1 and SMAD3/4 in a mouse model of breast carcinoma and at the invasive fronts of human breast cancer. We propose that activation of a SNAIL1-SMAD3/4 transcriptional complex represents a mechanism of gene repression during EMT.

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