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. 2022 Jul 15;21:146. doi: 10.1186/s12943-022-01607-8

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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. 11 — Proposed model for the potential function of circPOLR2A in cRCC progression. In the nucleus, circPOLR2A was derived from exons 9 and 10 of the POLR2A gene by backsplicing. After export to the cytoplasm, circPOLR2A interacted with UBE3C and PEBP1 proteins, and formed a circPOLR2A/UBE3C/PEBP1 protein-RNA ternary complex, which facilitated the ubiquitination and degradation of PEBP1 and further activated ERK signaling in cRCC progression. Furthermore, circPOLR2A could be modified by m6A, and the m6A reader YTHDF2 inhibited circPOLR2A expression in cRCC