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. 2023 Sep 13;42:239. doi: 10.1186/s13046-023-02813-y

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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. 8 — Circ-RAPGEF5 is involved in SUMOylation and promotes the SUMOylation of AKT. A-B Western blot analysis accessed the global SUMOylatoin level of Circ-RAPGEF5 silencing and upregulated in RBE and CCLP1 cells. C Western blot analysis detecting the global level of SUMOylation in Circ-RAPGEF5 knockdown and overexpression RBE cell while miR-3185 was silenced. D CO-IP assays to evaluate AKT SUMOylation level of Circ-RAPGEF5 knockdown and overexpression RBE cell. E CO-IP assays to testing SUMO-1 modified AKT level of Circ-RAPGEF5 knockdown and overexpression RBE cell. F SUMOylation modification analysis to explore the levels of AKT SUMOylation in Circ-RAPGEF5 knockdown and SAE1 overexpression RBE cell. G Hypothetical model for the carcinogenic mechanism of Circ-RAPGEF5. Circ-RAPGEF competitively sponges mir-3185 to stabilize SAE1, thereby promoting SUMOylation and tumor progression