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. 2021 Jun 9;12(6):598. doi: 10.1038/s41419-021-03868-5

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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. 3 — A m6A modifications play different roles in multiple cancers by influencing the maturation of miRNAs. m6A modification promotes miRNA maturation by recruiting DGCR8 to promote pri-miRNA processing or increasing pre-miRNA splicing by Dicer in different cancers. Furthermore, m6A modification can promote or inhibit the occurrence and development of tumors by affecting the maturation of miRNAs. HNRNPA2B1 has also been found to inhibit the shearing of some of the pri-miRNAs; however, the specific mechanism underlying this inhibition remains unclear in breast cancer. B miRNAs affect cancer progression by regulating m6A modification of mRNAs (METTL3, FTO, YTHDF1, and YTHDF2).