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Microbes-induced EMT at the crossroad of inflammation and cancer

It is noteworthy that bacterial or viral infections, and the resulting chronic inflammation, have been shown to predispose individuals to certain types of cancer. Remarkably, these microbes upregulated some transcription factors involved in the regulation of the epithelial to mesenchymal transition,...

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Detalles Bibliográficos
Autores principales: Hofman, Paul, Vouret-Craviari, Valérie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3427211/
https://www.ncbi.nlm.nih.gov/pubmed/22572828
http://dx.doi.org/10.4161/gmic.20288
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author Hofman, Paul
Vouret-Craviari, Valérie
author_facet Hofman, Paul
Vouret-Craviari, Valérie
author_sort Hofman, Paul
collection PubMed
description It is noteworthy that bacterial or viral infections, and the resulting chronic inflammation, have been shown to predispose individuals to certain types of cancer. Remarkably, these microbes upregulated some transcription factors involved in the regulation of the epithelial to mesenchymal transition, referred herein as EMT. EMT is a cellular process that consists in the conversion of epithelial cell phenotype to a mesenchymal phenotype. Under physiological conditions EMT is clearly important for embryogenesis, organ development, wound repair and tissue remodeling. However, EMT may also be activated under pathologic conditions, more particularly in carcinogenesis and metastatic progression. In this review, we make a parallel between microbes- and growth factors-induced transcription factors. A unifying EMT model then emerges that may help in understanding the development of microbial pathogenesis and in defining new potential future therapeutic strategy in treating diseases linked to infections.
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spelling pubmed-34272112012-08-27 Microbes-induced EMT at the crossroad of inflammation and cancer Hofman, Paul Vouret-Craviari, Valérie Gut Microbes Review It is noteworthy that bacterial or viral infections, and the resulting chronic inflammation, have been shown to predispose individuals to certain types of cancer. Remarkably, these microbes upregulated some transcription factors involved in the regulation of the epithelial to mesenchymal transition, referred herein as EMT. EMT is a cellular process that consists in the conversion of epithelial cell phenotype to a mesenchymal phenotype. Under physiological conditions EMT is clearly important for embryogenesis, organ development, wound repair and tissue remodeling. However, EMT may also be activated under pathologic conditions, more particularly in carcinogenesis and metastatic progression. In this review, we make a parallel between microbes- and growth factors-induced transcription factors. A unifying EMT model then emerges that may help in understanding the development of microbial pathogenesis and in defining new potential future therapeutic strategy in treating diseases linked to infections. Landes Bioscience 2012-05-01 /pmc/articles/PMC3427211/ /pubmed/22572828 http://dx.doi.org/10.4161/gmic.20288 Text en Copyright © 2012 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Review
Hofman, Paul
Vouret-Craviari, Valérie
Microbes-induced EMT at the crossroad of inflammation and cancer
title Microbes-induced EMT at the crossroad of inflammation and cancer
title_full Microbes-induced EMT at the crossroad of inflammation and cancer
title_fullStr Microbes-induced EMT at the crossroad of inflammation and cancer
title_full_unstemmed Microbes-induced EMT at the crossroad of inflammation and cancer
title_short Microbes-induced EMT at the crossroad of inflammation and cancer
title_sort microbes-induced emt at the crossroad of inflammation and cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3427211/
https://www.ncbi.nlm.nih.gov/pubmed/22572828
http://dx.doi.org/10.4161/gmic.20288
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