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A SNAIL1–SMAD3/4 tr...
A SNAIL1–SMAD3/4 transcriptional repressor complex promotes TGF‑β mediated epithelial–mesenchymal transition
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- Vincent, Theresa (author)
- Karolinska Institutet
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- Neve, Etienne P. A. (author)
- Karolinska Institutet
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- 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
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- Rojo, Federico (author)
- Oncology Department, Programa de Recerca en Càncer, IMIM-Hospital del Mar, 08003 Barcelona, Spain
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- Albanell, Joan (author)
- Oncology Department, Programa de Recerca en Càncer, IMIM-Hospital del Mar, 08003 Barcelona, Spain
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- Pietras, Kristian (author)
- Karolinska Institutet
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- Virtanen, Ismo (author)
- Institute of Biomedicine/Anatomy, FI‑00014, University of Helsinki, Finland
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- Philipson, Lennart (author)
- Karolinska Institutet
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- Leopold, Philip L. (author)
- Department of Chemistry, Chemical Biology, and Biomedical Engineering, Stevens Institute of Technology, New Jersey 07030, USA
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- Crystal, Ronald G. (author)
- Department of Genetic Medicine, Weill Medical College of Cornell University, New York 10065, USA
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- de Herreros, Antonio Garcia (author)
- Oncology Department, Programa de Recerca en Càncer, IMIM-Hospital del Mar, 08003 Barcelona, Spain
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- Moustakas, Aristidis (author)
- Uppsala universitet,Ludwiginstitutet för cancerforskning
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- Pettersson, Ralf F. (author)
- Ludwig Institute for Cancer Research, Stockholm Branch, 17177 Stockholm, Sweden
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- Fuxe, Jonas (author)
- Karolinska Institutet
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(creator_code:org_t)
- 2009-07-13
- 2009
- English.
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In: Nature Cell Biology. - : Springer Science and Business Media LLC. - 1465-7392 .- 1476-4679. ; 11:8, s. 943-950
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Abstract
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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.
Keyword
- MEDICINE
- MEDICIN
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- ref (subject category)
- art (subject category)
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Vincent, Theresa
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Neve, Etienne P. ...
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Johnson, Jill R.
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Kukalev, Alexand ...
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Rojo, Federico
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Albanell, Joan
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Pietras, Kristia ...
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Virtanen, Ismo
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Philipson, Lenna ...
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Leopold, Philip ...
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Crystal, Ronald ...
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de Herreros, Ant ...
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Moustakas, Arist ...
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Pettersson, Ralf ...
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Fuxe, Jonas
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Nature Cell Biol ...
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Uppsala University
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Karolinska Institutet