Epithelial to mesenchymal transition in tumor cells as consequence of phenotypic instability

During the last years many articles have reported epithelial-to-mesenchymal transitions (EMT) induced by a myriad of gene products either when added to the cell medium or when transfected. Molecularly the EMT is characterized by the up-regulation of transcriptional factors (EMT-TFs) repressing the e...

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Detalhes bibliográficos
Autor: García de Herreros, Antonio
Formato: artículo
Estado:Versión publicada
Fecha de publicación:2014
País:España
Recursos:Universitat Pompeu Fabra
Repositorio:Repositorio Digital de la UPF
OAI Identifier:oai:repositori.upf.edu:10230/58500
Acesso em linha:http://hdl.handle.net/10230/58500
http://dx.doi.org/10.3389/fcell.2014.00071
Access Level:acceso abierto
Palavra-chave:EMT
Snail1
E-cadherin
Self-amplification
Tumor instability
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oai_identifier_str oai:repositori.upf.edu:10230/58500
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spelling Epithelial to mesenchymal transition in tumor cells as consequence of phenotypic instabilityGarcía de Herreros, AntonioEMTSnail1E-cadherinSelf-amplificationTumor instabilityDuring the last years many articles have reported epithelial-to-mesenchymal transitions (EMT) induced by a myriad of gene products either when added to the cell medium or when transfected. Molecularly the EMT is characterized by the up-regulation of transcriptional factors (EMT-TFs) repressing the epithelial gene E-cadherin, a protein essential for the maintenance of the epithelial phenotype. These EMT-TFs are subjected to a complex regulation involving binary self-stimulatory loops, allowing the possibility of the amplification of input signals. The capability of EMT-TFs to promote an EMT is controlled by E-cadherin that limits the transcription of mesenchymal genes. We discuss here the differences between normal and tumor epithelial cells; in the latter a partial inactivation of E-cadherin function enables extracellular signals to be amplified and induce an EMT. This tumor cell phenotypic instability is exacerbated in cell culture conditions. Therefore, it is likely that many of the gene products reported to control this transition act only in very specific cell tumor cell lines; thus, in cells with an unstable phenotype due to pre-existing alterations in E-cadherin safeguard mechanism.Work in Antonio García de Herreros laboratory is supported by la Fundación Científica de la Asociación Española contra el Cáncer, Ministerio de Ciencia y Tecnología (SAF2013-48849-C2-1-R), Fundació La Marató de TV3, Fundación Rodríguez-Pascual and ISCIII/FEDER (RD12/0036/0005).Frontiers202320232014info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfapplication/pdfhttp://hdl.handle.net/10230/58500http://dx.doi.org/10.3389/fcell.2014.00071reponame:Repositorio Digital de la UPFinstname:Universitat Pompeu FabraInglésFrontiers in Cell and Developmental Biology. 2014 Dec 12;2:71info:eu-repo/grantAgreement/ES/1PE/SAF2013-48849-C2-1-R© 2014 García de Herreros. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.http://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:repositori.upf.edu:10230/585002026-06-12T07:21:37Z
dc.title.none.fl_str_mv Epithelial to mesenchymal transition in tumor cells as consequence of phenotypic instability
title Epithelial to mesenchymal transition in tumor cells as consequence of phenotypic instability
spellingShingle Epithelial to mesenchymal transition in tumor cells as consequence of phenotypic instability
García de Herreros, Antonio
EMT
Snail1
E-cadherin
Self-amplification
Tumor instability
title_short Epithelial to mesenchymal transition in tumor cells as consequence of phenotypic instability
title_full Epithelial to mesenchymal transition in tumor cells as consequence of phenotypic instability
title_fullStr Epithelial to mesenchymal transition in tumor cells as consequence of phenotypic instability
title_full_unstemmed Epithelial to mesenchymal transition in tumor cells as consequence of phenotypic instability
title_sort Epithelial to mesenchymal transition in tumor cells as consequence of phenotypic instability
dc.creator.none.fl_str_mv García de Herreros, Antonio
author García de Herreros, Antonio
author_facet García de Herreros, Antonio
author_role author
dc.subject.none.fl_str_mv EMT
Snail1
E-cadherin
Self-amplification
Tumor instability
topic EMT
Snail1
E-cadherin
Self-amplification
Tumor instability
description During the last years many articles have reported epithelial-to-mesenchymal transitions (EMT) induced by a myriad of gene products either when added to the cell medium or when transfected. Molecularly the EMT is characterized by the up-regulation of transcriptional factors (EMT-TFs) repressing the epithelial gene E-cadherin, a protein essential for the maintenance of the epithelial phenotype. These EMT-TFs are subjected to a complex regulation involving binary self-stimulatory loops, allowing the possibility of the amplification of input signals. The capability of EMT-TFs to promote an EMT is controlled by E-cadherin that limits the transcription of mesenchymal genes. We discuss here the differences between normal and tumor epithelial cells; in the latter a partial inactivation of E-cadherin function enables extracellular signals to be amplified and induce an EMT. This tumor cell phenotypic instability is exacerbated in cell culture conditions. Therefore, it is likely that many of the gene products reported to control this transition act only in very specific cell tumor cell lines; thus, in cells with an unstable phenotype due to pre-existing alterations in E-cadherin safeguard mechanism.
publishDate 2014
dc.date.none.fl_str_mv 2014
2023
2023
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/10230/58500
http://dx.doi.org/10.3389/fcell.2014.00071
url http://hdl.handle.net/10230/58500
http://dx.doi.org/10.3389/fcell.2014.00071
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Frontiers in Cell and Developmental Biology. 2014 Dec 12;2:71
info:eu-repo/grantAgreement/ES/1PE/SAF2013-48849-C2-1-R
dc.rights.none.fl_str_mv http://creativecommons.org/licenses/by/4.0/
info:eu-repo/semantics/openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Frontiers
publisher.none.fl_str_mv Frontiers
dc.source.none.fl_str_mv reponame:Repositorio Digital de la UPF
instname:Universitat Pompeu Fabra
instname_str Universitat Pompeu Fabra
reponame_str Repositorio Digital de la UPF
collection Repositorio Digital de la UPF
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15.228081

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