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. 2022 Aug 26;41:261. doi: 10.1186/s13046-022-02462-7

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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. 2 — m6A modification of circCCDC134. A and B m6A modification of circCCDC134 in the circPrimer and SRAMP prediction servers. C Motif analysis of the circCCDC134 methylation site. D ChIRP-MS showed that circCCDC134 cooperated with ALKBH5 and YTHDF2. E The GO results revealed that ALKBH5 and YTHDF2 may affect RNA stability. F and G ChIRP and H and I: RIP assays demonstrated that both ALKBH5 and YTHDF2 could interact with circCCDC134. J and K The qRT–PCR (24 tumour tissues) and IHC (5 pairs of CC tissues) results revealed that the expression of ALKBH5 was low in CC. L circCCDC134 expression was significantly negatively correlated with ALKBH5 expression in CC based on qPCR results. M and N qRT–PCR and actinomycin D assays showed that the expression and stability of circCCDC134 were decreased with ALKBH5 overexpression