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. 2018 Apr 3;9:614. doi: 10.3389/fmicb.2018.00614

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Copyright © 2018 Pasquereau-Kotula, Martins, Aymeric and Dramsi.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Two working models explaining Sgg association with colorectal cancer (CRC). (1) Sgg as a passenger bacterium: In pre-neoplastic epithelium, activation of the Wnt pathway leads to the downregulation of bile acids transporter Slc10A2 resulting in accumulation of bile acids- which in turn activates a specific “bacteriocin” enabling Sgg to kill related commensals (e.g., Enterococci). This local microbial imbalance can contribute to the development of CRC. (2) Sgg as a driver bacterium: High colonization of Sgg in pre-malignant epithelium can induce specific inflammatory responses (IL-1, COX-2, and IL-8) and increased cell proliferation associated with upregulation of β-catenin levels and its oncogenic downstream targets (c-Myc and cyclin D), thus accelerating transformation from pre-malignant to malignant epithelium.