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Implications of Gut Microbiota in Epithelial–Mesenchymal Transition and Cancer Progression: A Concise Review
SIMPLE SUMMARY: Recently, the interactions between microbiota and the host have been reported to induce the onset and progression of human cancer via epithelial–mesenchymal transition (EMT). In contrast, some microorganisms can protect against cancer growth, indicating an anticancer therapeutic acti...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9221329/ https://www.ncbi.nlm.nih.gov/pubmed/35740629 http://dx.doi.org/10.3390/cancers14122964 |
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author | Gupta, Ishita Pedersen, Shona Vranic, Semir Al Moustafa, Ala-Eddin |
author_facet | Gupta, Ishita Pedersen, Shona Vranic, Semir Al Moustafa, Ala-Eddin |
author_sort | Gupta, Ishita |
collection | PubMed |
description | SIMPLE SUMMARY: Recently, the interactions between microbiota and the host have been reported to induce the onset and progression of human cancer via epithelial–mesenchymal transition (EMT). In contrast, some microorganisms can protect against cancer growth, indicating an anticancer therapeutic action of such microbiota. In the review, we summarize findings from the literature, exploring the underlying mechanisms by which pathogenic microorganisms induce EMT. We also highlight the potential of exploiting these complex interactions for developing new biological therapies. ABSTRACT: Advancement in the development of molecular sequencing platforms has identified infectious bacteria or viruses that trigger the dysregulation of a set of genes inducing the epithelial–mesenchymal transition (EMT) event. EMT is essential for embryogenesis, wound repair, and organ development; meanwhile, during carcinogenesis, initiation of the EMT can promote cancer progression and metastasis. Recent studies have reported that interactions between the host and dysbiotic microbiota in different tissues and organs, such as the oral and nasal cavities, esophagus, stomach, gut, skin, and the reproductive tract, may provoke EMT. On the other hand, it is revealed that certain microorganisms display a protective role against cancer growth, indicative of possible therapeutic function. In this review, we summarize recent findings elucidating the underlying mechanisms of pathogenic microorganisms, especially the microbiota, in eliciting crucial regulator genes that induce EMT. Such an approach may help explain cancer progression and pave the way for developing novel preventive and therapeutic strategies. |
format | Online Article Text |
id | pubmed-9221329 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-92213292022-06-24 Implications of Gut Microbiota in Epithelial–Mesenchymal Transition and Cancer Progression: A Concise Review Gupta, Ishita Pedersen, Shona Vranic, Semir Al Moustafa, Ala-Eddin Cancers (Basel) Review SIMPLE SUMMARY: Recently, the interactions between microbiota and the host have been reported to induce the onset and progression of human cancer via epithelial–mesenchymal transition (EMT). In contrast, some microorganisms can protect against cancer growth, indicating an anticancer therapeutic action of such microbiota. In the review, we summarize findings from the literature, exploring the underlying mechanisms by which pathogenic microorganisms induce EMT. We also highlight the potential of exploiting these complex interactions for developing new biological therapies. ABSTRACT: Advancement in the development of molecular sequencing platforms has identified infectious bacteria or viruses that trigger the dysregulation of a set of genes inducing the epithelial–mesenchymal transition (EMT) event. EMT is essential for embryogenesis, wound repair, and organ development; meanwhile, during carcinogenesis, initiation of the EMT can promote cancer progression and metastasis. Recent studies have reported that interactions between the host and dysbiotic microbiota in different tissues and organs, such as the oral and nasal cavities, esophagus, stomach, gut, skin, and the reproductive tract, may provoke EMT. On the other hand, it is revealed that certain microorganisms display a protective role against cancer growth, indicative of possible therapeutic function. In this review, we summarize recent findings elucidating the underlying mechanisms of pathogenic microorganisms, especially the microbiota, in eliciting crucial regulator genes that induce EMT. Such an approach may help explain cancer progression and pave the way for developing novel preventive and therapeutic strategies. MDPI 2022-06-16 /pmc/articles/PMC9221329/ /pubmed/35740629 http://dx.doi.org/10.3390/cancers14122964 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Gupta, Ishita Pedersen, Shona Vranic, Semir Al Moustafa, Ala-Eddin Implications of Gut Microbiota in Epithelial–Mesenchymal Transition and Cancer Progression: A Concise Review |
title | Implications of Gut Microbiota in Epithelial–Mesenchymal Transition and Cancer Progression: A Concise Review |
title_full | Implications of Gut Microbiota in Epithelial–Mesenchymal Transition and Cancer Progression: A Concise Review |
title_fullStr | Implications of Gut Microbiota in Epithelial–Mesenchymal Transition and Cancer Progression: A Concise Review |
title_full_unstemmed | Implications of Gut Microbiota in Epithelial–Mesenchymal Transition and Cancer Progression: A Concise Review |
title_short | Implications of Gut Microbiota in Epithelial–Mesenchymal Transition and Cancer Progression: A Concise Review |
title_sort | implications of gut microbiota in epithelial–mesenchymal transition and cancer progression: a concise review |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9221329/ https://www.ncbi.nlm.nih.gov/pubmed/35740629 http://dx.doi.org/10.3390/cancers14122964 |
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