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Helicobacter pylori CagA and IL-1β Promote the Epithelial-to-Mesenchymal Transition in a Nontransformed Epithelial Cell Model

Gastric cancer is the third cause of cancer death worldwide and infection by Helicobacter pylori (H. pylori) is considered the most important risk factor, mainly by the activity of its virulence factor CagA. H. pylori/CagA-induced chronic inflammation triggers a series of gastric lesions of increase...

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Autores principales: Arévalo-Romero, Haruki, Meza, Isaura, Vallejo-Flores, Gabriela, Fuentes-Pananá, Ezequiel M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4971297/
https://www.ncbi.nlm.nih.gov/pubmed/27525003
http://dx.doi.org/10.1155/2016/4969163
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author Arévalo-Romero, Haruki
Meza, Isaura
Vallejo-Flores, Gabriela
Fuentes-Pananá, Ezequiel M.
author_facet Arévalo-Romero, Haruki
Meza, Isaura
Vallejo-Flores, Gabriela
Fuentes-Pananá, Ezequiel M.
author_sort Arévalo-Romero, Haruki
collection PubMed
description Gastric cancer is the third cause of cancer death worldwide and infection by Helicobacter pylori (H. pylori) is considered the most important risk factor, mainly by the activity of its virulence factor CagA. H. pylori/CagA-induced chronic inflammation triggers a series of gastric lesions of increased severity, starting with gastritis and ending with cancer. IL-1β has been associated with tumor development and invasiveness in different types of cancer, including gastric cancer. Currently, it is not clear if there is an association between CagA and IL-1β at a cellular level. In this study, we analyzed the effects of IL-1β and CagA on MCF-10A nontransformed cells. We found evidence that both CagA and IL-1β trigger the initiation of the epithelial-to-mesenchymal transition characterized by β-catenin nuclear translocation, increased expression of Snail1 and ZEB1, downregulation of CDH1, and morphological changes during MCF-10A acini formation. However, only CagA induced MMP9 activity and cell invasion. Our data support that IL-1β and CagA target the β-catenin pathway, with CagA leading to acquisition of a stage related to aggressive tumors.
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spelling pubmed-49712972016-08-14 Helicobacter pylori CagA and IL-1β Promote the Epithelial-to-Mesenchymal Transition in a Nontransformed Epithelial Cell Model Arévalo-Romero, Haruki Meza, Isaura Vallejo-Flores, Gabriela Fuentes-Pananá, Ezequiel M. Gastroenterol Res Pract Research Article Gastric cancer is the third cause of cancer death worldwide and infection by Helicobacter pylori (H. pylori) is considered the most important risk factor, mainly by the activity of its virulence factor CagA. H. pylori/CagA-induced chronic inflammation triggers a series of gastric lesions of increased severity, starting with gastritis and ending with cancer. IL-1β has been associated with tumor development and invasiveness in different types of cancer, including gastric cancer. Currently, it is not clear if there is an association between CagA and IL-1β at a cellular level. In this study, we analyzed the effects of IL-1β and CagA on MCF-10A nontransformed cells. We found evidence that both CagA and IL-1β trigger the initiation of the epithelial-to-mesenchymal transition characterized by β-catenin nuclear translocation, increased expression of Snail1 and ZEB1, downregulation of CDH1, and morphological changes during MCF-10A acini formation. However, only CagA induced MMP9 activity and cell invasion. Our data support that IL-1β and CagA target the β-catenin pathway, with CagA leading to acquisition of a stage related to aggressive tumors. Hindawi Publishing Corporation 2016 2016-07-20 /pmc/articles/PMC4971297/ /pubmed/27525003 http://dx.doi.org/10.1155/2016/4969163 Text en Copyright © 2016 Haruki Arévalo-Romero et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Arévalo-Romero, Haruki
Meza, Isaura
Vallejo-Flores, Gabriela
Fuentes-Pananá, Ezequiel M.
Helicobacter pylori CagA and IL-1β Promote the Epithelial-to-Mesenchymal Transition in a Nontransformed Epithelial Cell Model
title Helicobacter pylori CagA and IL-1β Promote the Epithelial-to-Mesenchymal Transition in a Nontransformed Epithelial Cell Model
title_full Helicobacter pylori CagA and IL-1β Promote the Epithelial-to-Mesenchymal Transition in a Nontransformed Epithelial Cell Model
title_fullStr Helicobacter pylori CagA and IL-1β Promote the Epithelial-to-Mesenchymal Transition in a Nontransformed Epithelial Cell Model
title_full_unstemmed Helicobacter pylori CagA and IL-1β Promote the Epithelial-to-Mesenchymal Transition in a Nontransformed Epithelial Cell Model
title_short Helicobacter pylori CagA and IL-1β Promote the Epithelial-to-Mesenchymal Transition in a Nontransformed Epithelial Cell Model
title_sort helicobacter pylori caga and il-1β promote the epithelial-to-mesenchymal transition in a nontransformed epithelial cell model
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4971297/
https://www.ncbi.nlm.nih.gov/pubmed/27525003
http://dx.doi.org/10.1155/2016/4969163
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