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. 2021 Feb 3;13(1):1848158. doi: 10.1080/19490976.2020.1848158

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© 2021 The Author(s). Published with license by Taylor & Francis Group, LLC.

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 work is properly cited.

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Figure 6. — Overview of the potential role of BFT in colo-rectal cancer

The interaction of the Bacteroides fragilis toxin (BFT) and the colonic epithelial cell (CEC) receptor results in E-cadherin cleavage which initiates a cascade of signaling events involving nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), mitogen-activated protein kinase (MAPK) and β-catenin. Consequent cellular events of the signals include the proliferation of proinflammatory cytokines (such as IL-8) that promote proinflammatory microenvironments, expression of the proto-oncogene, c-myc, and damage to DNA. Overall, the cellular events triggered by BFT result in CEC proliferation, mucosal inflammation, and potential metastasis.