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. 2023 Feb 21;14(2):148. doi: 10.1038/s41419-023-05670-x

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© The Author(s) 2023

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 — Low expression of METTL14 in CRC resulted in decreased m⁶A modification, which in turn reduced the recognition and binding of pri-miR-17 by YTHDC2, promoted the stability of pri-miR-17 mRNA, and increased the expression of miR-17-5p. Overexpressed miR-17-5p inhibited MFN2, leading to decreased mitochondrial fusion and enhanced mitochondrial fission and mitophagy, which ultimately induced drug resistance.