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. 2022 Apr 14;12:804689. doi: 10.3389/fcimb.2022.804689

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Copyright © 2022 Xing, Liao, Zhang, Zhang, Zhang, Zhang, Wang and Tang

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(s) 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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Butyrate produced by F. prausnitzii suppresses the proliferation of CRC cells by modulating miR-92a and miR-203. First, butyrate produced by F. prausnitzii suppressed oncogenic miR-92a overexpression in human CRC cells and detected a rapid decrease in the levels of c-MYC after butyrate treatment. miR-92a downregulation subsequently stimulated p57 expression, which is epigenetically silenced in cancer, blocks cell proliferation by promoting apoptosis, inhibiting angiogenesis and cell cycle arrest. In contrast, miR-203 expression is upregulated after butyrate treatment and consequently suppresses the proliferation of CRC cells via directly inhibiting NEDD9 expression. NEDD9, a significant tumor-promoting factor, can induce the EMT by activating JNK, thereby promoting tumor invasion and metastasis. Upregulated miR-203 induced by butyrate can also lower Hakai expression, eventually suppressing the proliferation of CRC cells.