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dc.creatorBlanco, D. (D.)-
dc.creatorVicent, S. (Silvestre)-
dc.creatorElizegi, E. (E.)-
dc.creatorPino, I. (Irene)-
dc.creatorFraga, M.F. (Mario F.)-
dc.creatorEsteller, M. (Manel)-
dc.creatorSaffiotti, U. (Umberto)-
dc.creatorLecanda, F. (Fernando)-
dc.creatorMontuenga-Badia, L.M. (Luis M.)-
dc.date.accessioned2011-08-19T11:15:50Z-
dc.date.available2011-08-19T11:15:50Z-
dc.date.issued2004-
dc.identifier.citationBlanco D, Vicent S, Elizegi E, Pino I, Fraga MF, Esteller M, et al. Altered expression of adhesion molecules and epithelial-mesenchymal transition in silica-induced rat lung carcinogenesis. Lab Invest 2004 Aug;84(8):999-1012.es_ES
dc.identifier.issn1530-0307-
dc.identifier.urihttps://hdl.handle.net/10171/18809-
dc.description.abstractLoss of the epithelial phenotype and disruption of adhesion molecules is a hallmark in the epithelial-mesenchymal transition (EMT) reported in several types of cancer. Most of the studies about the relevance of adhesion and junction molecules in lung cancer have been performed using established tumors or in vitro models. The sequential molecular events leading to EMT during lung cancer progression are still not well understood. We have used a rat model for multistep lung carcinogenesis to study the status of adherens and tight junction proteins and mesenchymal markers during EMT. After silica-induced chronic inflammation, rats sequentially develop epithelial hyperplasia, preneoplastic lesions, and tumors such as adenocarcinomas and squamous cell carcinomas. In comparison with normal and hyperplastic bronchiolar epithelium and with hyperplastic alveolar type II cells, the expression levels of E-cadherin, alpha-catenin and beta-catenin were significantly reduced in adenomatoid preneoplastic lesions and in late tumors. The loss of E-cadherin in tumors was associated with its promoter hypermethylation. alpha- and beta-catenin dysregulation lead to cytoplasmic accumulation in some carcinomas. No nuclear beta-catenin localization was found at any stage of any preneoplastic or neoplastic lesion. Zonula occludens protein-1 was markedly decreased in 66% of adenocarcinomas and in 100% squamous cell carcinomas. The mesenchymal-associated proteins N-cadherin and vimentin were analyzed as markers for EMT. N-cadherin was de novo expressed in 32% of adenocarcinomas and 33% of squamous cell carcinomas. Vimentin-positive tumor cells were found in 35% of adenocarcinomas and 88% of squamous cell carcinomas. Mesenchymal markers were absent in precursor lesions, both hyperplastic and adenomatoid. The present results show that silica-induced rat lung carcinogenesis is a good model to study EMT in vivo, and also provide in vivo evidence suggesting that the changes in cell-cell adhesion molecules are an early event in lung carcinogenesis, while EMT occurs at a later stage.es_ES
dc.language.isoenges_ES
dc.publisherNature Publishing Groupes_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.subjectAdhesion moleculeses_ES
dc.subjectCadherines_ES
dc.subjectCatenines_ES
dc.subjectTight junctiones_ES
dc.subjectLung canceres_ES
dc.subjectEMTes_ES
dc.subjectDNA methylationes_ES
dc.titleAltered expression of adhesion molecules and epithelial-mesenchymal transition in silica-induced rat lung carcinogenesises_ES
dc.typeArticuloes_ES
dc.relation.publisherversionhttp://www.nature.com/labinvest/journal/v84/n8/full/3700129a.htmles_ES

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