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The Mechanism of Bacteroides fragilis Toxin Contributes to Colon Cancer Formation
The Bacteroides fragilis (B. fragilis) produce biofilm for colonisation in the intestinal tract can cause a series of inflammatory reactions due to B. fragilis toxin (BFT) which can lead to chronic intestinal inflammation and tissue injury and play a crucial role leading to colorectal cancer (CRC)....
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Penerbit Universiti Sains Malaysia
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7444842/ https://www.ncbi.nlm.nih.gov/pubmed/32863742 http://dx.doi.org/10.21315/mjms2020.27.4.2 |
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author | Cheng, Wai Teng Kantilal, Haresh Kumar Davamani, Fabian |
author_facet | Cheng, Wai Teng Kantilal, Haresh Kumar Davamani, Fabian |
author_sort | Cheng, Wai Teng |
collection | PubMed |
description | The Bacteroides fragilis (B. fragilis) produce biofilm for colonisation in the intestinal tract can cause a series of inflammatory reactions due to B. fragilis toxin (BFT) which can lead to chronic intestinal inflammation and tissue injury and play a crucial role leading to colorectal cancer (CRC). The enterotoxigenic B. fragilis (ETBF) forms biofilm and produce toxin and play a role in CRC, whereas the non-toxigenic B. fragilis (NTBF) does not produce toxin. The ETBF triggers the expression of cyclooxygenase (COX)-2 that releases PGE2 for inducing inflammation and control cell proliferation. From chronic intestinal inflammation to cancer development, it involves signal transducers and activators of transcription (STAT)3 activation. STAT3 activates by the interaction between epithelial cells and BFT. Thus, regulatory T-cell (Tregs) will activates and reduce interleukin (IL)-2 amount. As the level of IL-2 drops, T-helper (T(h)17) cells are generated leading to increase in IL-17 levels. IL-17 is implicated in early intestinal inflammation and promotes cancer cell survival and proliferation and consequently triggers IL-6 production that activate STAT3 pathway. Additionally, BFT degrades E-cadherin, hence alteration of signalling pathways can upregulate spermine oxidase leading to cell morphology and promote carcinogenesis and irreversible DNA damage. Patient with familial adenomatous polyposis (FAP) disease displays a high level of tumour load in the colon. This disease is caused by germline mutation of the adenomatous polyposis coli (APC) gene that increases bacterial adherence to the mucosa layer. Mutated-APC gene genotype with ETBF increases the chances of CRC development. Therefore, the colonisation of the ETBF in the intestinal tract depicts tumour aetiology can result in risk of hostility and effect on human health. |
format | Online Article Text |
id | pubmed-7444842 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Penerbit Universiti Sains Malaysia |
record_format | MEDLINE/PubMed |
spelling | pubmed-74448422020-08-27 The Mechanism of Bacteroides fragilis Toxin Contributes to Colon Cancer Formation Cheng, Wai Teng Kantilal, Haresh Kumar Davamani, Fabian Malays J Med Sci Review Article The Bacteroides fragilis (B. fragilis) produce biofilm for colonisation in the intestinal tract can cause a series of inflammatory reactions due to B. fragilis toxin (BFT) which can lead to chronic intestinal inflammation and tissue injury and play a crucial role leading to colorectal cancer (CRC). The enterotoxigenic B. fragilis (ETBF) forms biofilm and produce toxin and play a role in CRC, whereas the non-toxigenic B. fragilis (NTBF) does not produce toxin. The ETBF triggers the expression of cyclooxygenase (COX)-2 that releases PGE2 for inducing inflammation and control cell proliferation. From chronic intestinal inflammation to cancer development, it involves signal transducers and activators of transcription (STAT)3 activation. STAT3 activates by the interaction between epithelial cells and BFT. Thus, regulatory T-cell (Tregs) will activates and reduce interleukin (IL)-2 amount. As the level of IL-2 drops, T-helper (T(h)17) cells are generated leading to increase in IL-17 levels. IL-17 is implicated in early intestinal inflammation and promotes cancer cell survival and proliferation and consequently triggers IL-6 production that activate STAT3 pathway. Additionally, BFT degrades E-cadherin, hence alteration of signalling pathways can upregulate spermine oxidase leading to cell morphology and promote carcinogenesis and irreversible DNA damage. Patient with familial adenomatous polyposis (FAP) disease displays a high level of tumour load in the colon. This disease is caused by germline mutation of the adenomatous polyposis coli (APC) gene that increases bacterial adherence to the mucosa layer. Mutated-APC gene genotype with ETBF increases the chances of CRC development. Therefore, the colonisation of the ETBF in the intestinal tract depicts tumour aetiology can result in risk of hostility and effect on human health. Penerbit Universiti Sains Malaysia 2020-07 2020-08-19 /pmc/articles/PMC7444842/ /pubmed/32863742 http://dx.doi.org/10.21315/mjms2020.27.4.2 Text en © Penerbit Universiti Sains Malaysia, 2020 This work is licensed under the terms of the Creative Commons Attribution (CC BY) (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Article Cheng, Wai Teng Kantilal, Haresh Kumar Davamani, Fabian The Mechanism of Bacteroides fragilis Toxin Contributes to Colon Cancer Formation |
title | The Mechanism of Bacteroides fragilis Toxin Contributes to Colon Cancer Formation |
title_full | The Mechanism of Bacteroides fragilis Toxin Contributes to Colon Cancer Formation |
title_fullStr | The Mechanism of Bacteroides fragilis Toxin Contributes to Colon Cancer Formation |
title_full_unstemmed | The Mechanism of Bacteroides fragilis Toxin Contributes to Colon Cancer Formation |
title_short | The Mechanism of Bacteroides fragilis Toxin Contributes to Colon Cancer Formation |
title_sort | mechanism of bacteroides fragilis toxin contributes to colon cancer formation |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7444842/ https://www.ncbi.nlm.nih.gov/pubmed/32863742 http://dx.doi.org/10.21315/mjms2020.27.4.2 |
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