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dc.contributor.authorOcaña, Oscar H.-
dc.contributor.authorCórcoles, Rebeca-
dc.contributor.authorFabra, Àngels-
dc.contributor.authorMoreno-Bueno, Gema-
dc.contributor.authorAcloque, Hervé-
dc.contributor.authorVega, Sonia-
dc.contributor.authorBarrallo-Gimeno, Alejandro-
dc.contributor.authorCano, Amparo-
dc.contributor.authorNieto, M. Ángela-
dc.identifierdoi: 10.1016/j.ccr.2012.10.012-
dc.identifierissn: 1535-6108-
dc.identifiere-issn: 1878-3686-
dc.identifier.citationCancer Cell 22(6): 709-724 (2012)-
dc.description.abstractThe epithelial-mesenchymal transition (EMT) is required in the embryo for the formation of tissues for which cells originate far from their final destination. Carcinoma cells hijack this program for tumor dissemination. The relevance of the EMT in cancer is still debated because it is unclear how these migratory cells colonize distant tissues to form macrometastases. We show that the homeobox factor Prrx1 is an EMT inducer conferring migratory and invasive properties. The loss of Prrx1 is required for cancer cells to metastasize in vivo, which revert to the epithelial phenotype concomitant with the acquisition of stem cell properties. Thus, unlike the classical EMT transcription factors, Prrx1 uncouples EMT and stemness, and is a biomarker associated with patient survival and lack of metastasis. © 2012 Elsevier Inc.-
dc.description.sponsorshipThis work has been supported by grants from the Spanish Ministry of Science and Innovation BFU2008-01042 (to M.A.N.), SAF2010-21143 (to A.C.), and CONSOLIDER-INGENIO 2010 CSD2007-00017 to both labs. A grant from the Spanish Fondo de Investigaciones Sanitarias (FIS PS09/00373) supports A.F.’s lab and CONSOLIDER-INGENIO 2010 CSD2007-00023 and Generalitat Valenciana (Prometeo 2008/049 and ISIC/2012/010) also support M.A.N.’s lab.-
dc.publisherCell Press-
dc.titleMetastatic colonization requires the repression of the epithelial-mesenchymal transition inducer Prrx1-
dc.description.versionPeer Reviewed-
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