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Gut Microbiota and Colon Cancer: A Role for Bacterial Protein Toxins?
Accumulating evidence indicates that the human intestinal microbiota can contribute to the etiology of colorectal cancer. Triggering factors, including inflammation and bacterial infections, may favor the shift of the gut microbiota from a mutualistic to a pro-carcinogenic configuration. In this con...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7504354/ https://www.ncbi.nlm.nih.gov/pubmed/32867331 http://dx.doi.org/10.3390/ijms21176201 |
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author | Fiorentini, Carla Carlini, Francesca Germinario, Elena Angela Pia Maroccia, Zaira Travaglione, Sara Fabbri, Alessia |
author_facet | Fiorentini, Carla Carlini, Francesca Germinario, Elena Angela Pia Maroccia, Zaira Travaglione, Sara Fabbri, Alessia |
author_sort | Fiorentini, Carla |
collection | PubMed |
description | Accumulating evidence indicates that the human intestinal microbiota can contribute to the etiology of colorectal cancer. Triggering factors, including inflammation and bacterial infections, may favor the shift of the gut microbiota from a mutualistic to a pro-carcinogenic configuration. In this context, certain bacterial pathogens can exert a pro-tumoral activity by producing enzymatically-active protein toxins that either directly induce host cell DNA damage or interfere with essential host cell signaling pathways involved in cell proliferation, apoptosis, and inflammation. This review is focused on those toxins that, by mimicking carcinogens and cancer promoters, could represent a paradigm for bacterially induced carcinogenesis. |
format | Online Article Text |
id | pubmed-7504354 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-75043542020-09-24 Gut Microbiota and Colon Cancer: A Role for Bacterial Protein Toxins? Fiorentini, Carla Carlini, Francesca Germinario, Elena Angela Pia Maroccia, Zaira Travaglione, Sara Fabbri, Alessia Int J Mol Sci Review Accumulating evidence indicates that the human intestinal microbiota can contribute to the etiology of colorectal cancer. Triggering factors, including inflammation and bacterial infections, may favor the shift of the gut microbiota from a mutualistic to a pro-carcinogenic configuration. In this context, certain bacterial pathogens can exert a pro-tumoral activity by producing enzymatically-active protein toxins that either directly induce host cell DNA damage or interfere with essential host cell signaling pathways involved in cell proliferation, apoptosis, and inflammation. This review is focused on those toxins that, by mimicking carcinogens and cancer promoters, could represent a paradigm for bacterially induced carcinogenesis. MDPI 2020-08-27 /pmc/articles/PMC7504354/ /pubmed/32867331 http://dx.doi.org/10.3390/ijms21176201 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Fiorentini, Carla Carlini, Francesca Germinario, Elena Angela Pia Maroccia, Zaira Travaglione, Sara Fabbri, Alessia Gut Microbiota and Colon Cancer: A Role for Bacterial Protein Toxins? |
title | Gut Microbiota and Colon Cancer: A Role for Bacterial Protein Toxins? |
title_full | Gut Microbiota and Colon Cancer: A Role for Bacterial Protein Toxins? |
title_fullStr | Gut Microbiota and Colon Cancer: A Role for Bacterial Protein Toxins? |
title_full_unstemmed | Gut Microbiota and Colon Cancer: A Role for Bacterial Protein Toxins? |
title_short | Gut Microbiota and Colon Cancer: A Role for Bacterial Protein Toxins? |
title_sort | gut microbiota and colon cancer: a role for bacterial protein toxins? |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7504354/ https://www.ncbi.nlm.nih.gov/pubmed/32867331 http://dx.doi.org/10.3390/ijms21176201 |
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