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. 2024 Jan 24;31(4):562–573. doi: 10.1038/s41417-024-00731-5

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© The Author(s) 2024

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. 4 — A RIP assays showed the binding between the METTL3 protein and RanGAP1 mRNA. B The protein levels of RanGAP1 in METTL3 knockdown CRC cells. C m6A motifs were identified by MeRIP-seq in METTL3 silenced HCT116 and control group. D SRAMP website showed the potential site of m6A modification of RanGAP1 mRNA. E METTL3 knockdown reduced m6A modification of RanGAP1 mRNA in HCT116 cells. F Luciferase reporter assays showed the m6A modification affect the expression of RanGAP1. G RNA stability of RanGAP1 mRNA in downregulating METTL3 CRC cells and control cells after giving actinomycin D (5 μg/mL). H RIP assays showed the binding between the YTHDF1 protein and RanGAP1 mRNA in DLD1 cells. I The protein levels of RanGAP1 in YTHDF1 silenced CRC cells. J The protein expression levels in CRC cells transfected stably with the shNC+Control, shMETTL3+Control, shMETTL3+RanGAP1, shYTHDF1+Control and shYTHDF1 + RanGAP1. K–N The downtrend of proliferation, migration and invasion by shMETTL3 or shYTHDF1 of HCT116 and DLD1 were sectionally recurred because of RanGAP1 overexpressing.