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β7 integrins contribute to intestinal tumor growth in mice

The gut homing receptor integrin α4β7 is essential for the migration of pro-inflammatory T cells into the gut mucosa. Since intestinal neoplasia has been associated with chronic inflammation, we investigated whether interfering with gut-homing affects intestinal tumorigenesis. Using chemically induc...

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Autores principales: Das, Srustidhar, Doñas, Cristian, Akeus, Paulina, Quiding-Järbrink, Marianne, Mora, J. Rodrigo, Villablanca, Eduardo J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6147474/
https://www.ncbi.nlm.nih.gov/pubmed/30235302
http://dx.doi.org/10.1371/journal.pone.0204181
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author Das, Srustidhar
Doñas, Cristian
Akeus, Paulina
Quiding-Järbrink, Marianne
Mora, J. Rodrigo
Villablanca, Eduardo J.
author_facet Das, Srustidhar
Doñas, Cristian
Akeus, Paulina
Quiding-Järbrink, Marianne
Mora, J. Rodrigo
Villablanca, Eduardo J.
author_sort Das, Srustidhar
collection PubMed
description The gut homing receptor integrin α4β7 is essential for the migration of pro-inflammatory T cells into the gut mucosa. Since intestinal neoplasia has been associated with chronic inflammation, we investigated whether interfering with gut-homing affects intestinal tumorigenesis. Using chemically induced and spontaneous intestinal tumor models we showed that lack of β7 integrin significantly impairs tumor growth without affecting tumor frequencies, with a mild translatable effect on overall survival. This correlates with human data showing lower MAdCAM-1 expression and disease-free survival in colorectal cancer patients. Thus, paradoxically in contrast to extra-intestinal tumors, blocking migration of immune cells into the gut might have a positive therapeutic effect on intestinal neoplasia.
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spelling pubmed-61474742018-10-08 β7 integrins contribute to intestinal tumor growth in mice Das, Srustidhar Doñas, Cristian Akeus, Paulina Quiding-Järbrink, Marianne Mora, J. Rodrigo Villablanca, Eduardo J. PLoS One Research Article The gut homing receptor integrin α4β7 is essential for the migration of pro-inflammatory T cells into the gut mucosa. Since intestinal neoplasia has been associated with chronic inflammation, we investigated whether interfering with gut-homing affects intestinal tumorigenesis. Using chemically induced and spontaneous intestinal tumor models we showed that lack of β7 integrin significantly impairs tumor growth without affecting tumor frequencies, with a mild translatable effect on overall survival. This correlates with human data showing lower MAdCAM-1 expression and disease-free survival in colorectal cancer patients. Thus, paradoxically in contrast to extra-intestinal tumors, blocking migration of immune cells into the gut might have a positive therapeutic effect on intestinal neoplasia. Public Library of Science 2018-09-20 /pmc/articles/PMC6147474/ /pubmed/30235302 http://dx.doi.org/10.1371/journal.pone.0204181 Text en © 2018 Das et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Das, Srustidhar
Doñas, Cristian
Akeus, Paulina
Quiding-Järbrink, Marianne
Mora, J. Rodrigo
Villablanca, Eduardo J.
β7 integrins contribute to intestinal tumor growth in mice
title β7 integrins contribute to intestinal tumor growth in mice
title_full β7 integrins contribute to intestinal tumor growth in mice
title_fullStr β7 integrins contribute to intestinal tumor growth in mice
title_full_unstemmed β7 integrins contribute to intestinal tumor growth in mice
title_short β7 integrins contribute to intestinal tumor growth in mice
title_sort β7 integrins contribute to intestinal tumor growth in mice
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6147474/
https://www.ncbi.nlm.nih.gov/pubmed/30235302
http://dx.doi.org/10.1371/journal.pone.0204181
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