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A SNAIL1–SMAD3/4 tr...
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Vincent, TheresaKarolinska Institutet
(författare)
A SNAIL1–SMAD3/4 transcriptional repressor complex promotes TGF‑β mediated epithelial–mesenchymal transition
- Artikel/kapitelEngelska2009
Förlag, utgivningsår, omfång ...
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2009-07-13
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Springer Science and Business Media LLC,2009
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printrdacarrier
Nummerbeteckningar
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LIBRIS-ID:oai:DiVA.org:uu-108560
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-108560URI
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https://doi.org/10.1038/ncb1905DOI
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http://kipublications.ki.se/Default.aspx?queryparsed=id:119170689URI
Kompletterande språkuppgifter
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Språk:engelska
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Sammanfattning på:engelska
Ingår i deldatabas
Klassifikation
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Ämneskategori:ref swepub-contenttype
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Ämneskategori:art swepub-publicationtype
Anmärkningar
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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.
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
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Neve, Etienne P. A.Karolinska Institutet
(författare)
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Johnson, Jill R.Department of Cell and Molecular Biology, Karolinska Institute, 17177 Stockholm, Sweden
(författare)
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Kukalev, AlexanderDepartment of Cell and Molecular Biology, Karolinska Institute, 17177 Stockholm, Sweden
(författare)
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Rojo, FedericoOncology Department, Programa de Recerca en Càncer, IMIM-Hospital del Mar, 08003 Barcelona, Spain
(författare)
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Albanell, JoanOncology Department, Programa de Recerca en Càncer, IMIM-Hospital del Mar, 08003 Barcelona, Spain
(författare)
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Pietras, KristianKarolinska Institutet
(författare)
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Virtanen, IsmoInstitute of Biomedicine/Anatomy, FI‑00014, University of Helsinki, Finland
(författare)
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Philipson, LennartKarolinska Institutet
(författare)
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Leopold, Philip L.Department of Chemistry, Chemical Biology, and Biomedical Engineering, Stevens Institute of Technology, New Jersey 07030, USA
(författare)
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Crystal, Ronald G.Department of Genetic Medicine, Weill Medical College of Cornell University, New York 10065, USA
(författare)
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de Herreros, Antonio GarciaOncology Department, Programa de Recerca en Càncer, IMIM-Hospital del Mar, 08003 Barcelona, Spain
(författare)
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Moustakas, AristidisUppsala universitet,Ludwiginstitutet för cancerforskning(Swepub:uu)arimo287
(författare)
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Pettersson, Ralf F.Ludwig Institute for Cancer Research, Stockholm Branch, 17177 Stockholm, Sweden
(författare)
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Fuxe, JonasKarolinska Institutet
(författare)
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Karolinska InstitutetDepartment of Cell and Molecular Biology, Karolinska Institute, 17177 Stockholm, Sweden
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Nature Cell Biology: Springer Science and Business Media LLC11:8, s. 943-9501465-73921476-4679
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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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visa fler...
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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 universitet
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Karolinska Institutet