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. 2022 Nov 24;41:330. doi: 10.1186/s13046-022-02528-6

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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. 7 — ALKBH5 regulates UBR7 expression through m6A modification. A UBR7 expression was positively correlated with ALKBH5 expression in an analysis of TCGA data. B-E qRT-PCR and western blot analysis of ALBKH5 and UBR7 upon ALKBH5 silencing or overexpression. F, G RIP-qPCR showed the enrichment of UBR7 m⁶A upon ALKBH5 silencing or overexpression. H The decay rate of UBR7 mRNA in cells treated with 2.5 mmol/L actinomycin D for indicated times upon ALKBH5 silencing or overexpression. Data are shown as the mean ± SD. ^*P < 0.05; ^**P < 0.01