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. 2023 Nov 28;24:300. doi: 10.1186/s12931-023-02606-z

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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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — METTL3-mediated m6A RNA methylation promotes pri-miR-21 processing by DGCR8. A Prediction score distribution of the potential m6A modification sites along the pri-miR-21 sequence. B RIP-qPCR analysis of pri-miR-21 enrichment by METTL3, m6A and DGCR8 in LR-MSCs with or without METTL3 silencing. (C-D) qRT‒PCR analysis of pri-miR-21 (C) and miR-21 (D) expression levels in the METTL3 overexpression group or METTL3 silencing group compared to the control. E, F qRT‒PCR analysis of pri-miR-21 (E) and miR-21 (F) expression levels in the following four cases: control group, METTL3 silencing group, TGF-β1-treated group, and METTL3 silencing group treated with TGF-β1. U6 and β-Actin were used as reference genes. **P < 0.01