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Signaling networks guiding epithelial-mesenchymal transitions during embryogenesis and cancer progression
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , Ludwig Institute for Cancer Research.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , Ludwig Institute for Cancer Research.
2007 (English)In: Cancer Science, ISSN 1347-9032, E-ISSN 1349-7006, Vol. 98, no 10, 1512-1520 p.Article, review/survey (Refereed) Published
Abstract [en]

Epithelial–mesenchymal transition (EMT) describes the differentiation switch between polarized epithelial cells and contractile and motile mesenchymal cells, and facilitates cell movements and generation of new tissue types during embryogenesis. Many secreted polypeptides are implicated in the EMT process and their corresponding intracellular transduction pathways form highly interconnected networks. Transforming growth factor-β, Wnt, Notch and growth factors acting through tyrosine kinase receptors induce EMT and often act in a sequential manner. Such growth factors orchestrate the concerted regulation of an elaborate gene program and a complex protein network, needed for establishment of new mesenchymal phenotypes after disassembly of the main elements of epithelial architecture, such as desmosomes, as well as tight, adherens and gap junctions. EMT of tumor cells occurs during cancer progression and possibly generates cell types of the tumor stroma, such as cancer-associated myofibroblasts. EMT contributes to new tumor cell properties required for invasiveness and vascular intravasation during metastasis. Here we present some of the current mechanisms that mediate the process of EMT and discuss their relevance to cancer progression.

Place, publisher, year, edition, pages
2007. Vol. 98, no 10, 1512-1520 p.
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-11308DOI: 10.1111/j.1349-7006.2007.00550.xISI: 000249039900002PubMedID: 17645776OAI: oai:DiVA.org:uu-11308DiVA: diva2:39076
Available from: 2007-08-30 Created: 2007-08-30 Last updated: 2017-12-11Bibliographically approved

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Moustakas, AristidisHeldin, Carl-Henrik

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