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dc.contributor.authorSarrió, David-
dc.contributor.authorPalacios Calvo, José-
dc.contributor.authorHergueta-Redondo, Marta-
dc.contributor.authorGómez-López, Gonzalo-
dc.contributor.authorCano, Amparo-
dc.contributor.authorMoreno-Bueno, Gema-
dc.date.accessioned2009-03-26T10:08:56Z-
dc.date.available2009-03-26T10:08:56Z-
dc.date.issued2009-03-03-
dc.identifier.citationBMC Cancer 9: 74 (2009)en_US
dc.identifier.issn1471-2407-
dc.identifier.urihttp://hdl.handle.net/10261/11853-
dc.description14 páginas, 4 figuras.-- PMID: 19257890 [PubMed].-- PMCID: PMC2656544.-- Información adicional (Suppl. files S1-S6) disponible en: http://www.biomedcentral.com/1471-2407/9/74/additional/en_US
dc.descriptionAdditional files: 1. Wound healing assay 231-control cells.-- 2. Wound healing assay 231-E-cadherin cells.-- 3. Wound healing assay 231-P-cadherin cells.-- 4. Complete list of genes modulated by E-cadherin and/or P-cadherin (at least 2 fold with respect to control cells) in 231 cells.-- 5. Potential signaling networks mediated by E-cadherin-regulated genes at the biological process level.-- 6. Potential signaling networks mediated by P-cadherin-regulated genes at the biological process level.-
dc.description.abstract[Background]: Alterations in the cadherin-catenin adhesion complexes are involved in tumor initiation, progression and metastasis. However, the functional implication of distinct cadherin types in breast cancer biology is still poorly understood.en_US
dc.description.abstract[Methods]: To compare the functional role of E-cadherin and P-cadherin in invasive breast cancer, we stably transfected these molecules into the MDA-MB-231 cell line, and investigated their effects on motility, invasion and gene expression regulation.en_US
dc.description.abstract[Results]: Expression of either E- and P-cadherin significantly increased cell aggregation and induced a switch from fibroblastic to epithelial morphology. Although expression of these cadherins did not completely reverse the mesenchymal phenotype of MDA-MB-231 cells, both E- and P-cadherin decreased fibroblast-like migration and invasion through extracellular matrix in a similar way. Moreover, microarray gene expression analysis of MDA-MB-231 cells after expression of E- and P-cadherins revealed that these molecules can activate signaling pathways leading to significant changes in gene expression. Although the expression patterns induced by E- and P-cadherin showed more similarities than differences, 40 genes were differentially modified by the expression of either cadherin type.en_US
dc.description.abstract[Conclusion]: E- and P-cadherin have similar functional consequences on the phenotype and invasive behavior of MDA-MB-231 cells. Moreover, we demonstrate for the first time that these cadherins can induce both common and specific gene expression programs on invasive breast cancer cells. Importantly, these identified genes are potential targets for future studies on the functional consequences of altered cadherin expression in human breast cancer.en_US
dc.description.sponsorshipThis work has been supported by grants from the Fundación Mutua Madrileña (2006) and SAF2007-63075 to GMB; SAF 2007-63051 to AC; PI051890 and SAF2004-08258-C02-01 to JP. David Sarrió currently is a recipient of a Marie Curie Intra-European Fellowship of the European Commission (PIEF-GA-2008-221083). Gema Moreno-Bueno is a junior investigator of the "Ramón y Cajal Program" of the Spanish Ministry of Education and Science (2004).en_US
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dc.format.mimetypeapplication/pdf-
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dc.language.isoengen_US
dc.publisherBioMed Centralen_US
dc.relation.isversionofPublisher’s version-
dc.rightsopenAccessen_US
dc.subjectInvasive breast canceren_US
dc.subjectE-cadherinen_US
dc.subjectP-cadherinen_US
dc.subjectCadherin-catenin adhesion complexesen_US
dc.subjectFibroblast-like migrationen_US
dc.subjectGene expressionen_US
dc.titleFunctional characterization of E- and P-cadherin in invasive breast cancer cellsen_US
dc.typeartículoen_US
dc.identifier.doi10.1186/1471-2407-9-74-
dc.description.peerreviewedPeer revieweden_US
dc.relation.publisherversionhttp://dx.doi.org/10.1186/1471-2407-9-74en_US
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