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. 2021 Dec 8;7:379. doi: 10.1038/s41420-021-00715-6

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© The Author(s) 2021

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. 8 — miR-181d directly targets OGT and inhibits the expression of OGT, thereby inhibiting the glycosylation of KEAP1, reducing the ubiquitination, and degradation of NRF2 and promoting the expression of NRF2. By this mechanism, the viability of OC cells is promoted while cell apoptosis is suppressed, ultimately inducing the chemoresistance of OC.