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. 2022 Apr 2;21:93. doi: 10.1186/s12943-022-01537-5

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© The Author(s) 2022

Open AccessThis 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 — IGF2BP1 mediated circMAP3K4 translation by recognizing m6A modifications. A Western blot analysis for circMAP3K4-455aa expression after overexpressing ALKBH5 or FTO (left panel) or knocking down METTL3 (right panel). B Silver staining of circMAP3K4 probe pull down products. C LC–MS/MS and immunoblot assay for circMAP3K4 interaction with IGF2BP1 or IGF2BP2, respectively. D, E IGF2BP1 RIP (D) and IF-FISH (E) verified the IGF2BP1 interaction with circMAP3K4. F MeRIP revealed abundant m6A modification of circMAP3K4, normalized to IgG. G RNA pull down assay verification that the interaction between IGF2BP1 and circMAP3K4 depends on m6A modification. H IGF2BP1 knockdown decreased circMAP3K4-455aa expression. I, J Immunoblot analyses and western blot of complexes pulled down by the circMAP3K4 probe with various m6A site mutants. cMAP3K4 or cMAP, circMAP3K4