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. 2018 Aug 9;38(3):301–316. doi: 10.1038/s41388-018-0435-5

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — Schematic model depicting that miR-101/O-GlcNAcylation/EZH2 signaling promotes metastasis in CRC. In colorectal cancer tissues, a low miR-101 level leads to an increase in the protein levels of OGT and EZH2. Meanwhile, OGT enhances the stability and function of EZH2 by O-GlcNAcylation. As a result, EZH2 promotes the tri-methylation of H3K27 in the miR-101 promoter region, which further reduces the level of miR-101 in cancer tissues. In brief, the miR-101-O-GlcNAc/EZH2 regulatory feedback circuit promotes metastasis in CRC