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. 2022 Jun 23;21:135. doi: 10.1186/s12943-022-01600-1

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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 — circEXOC6B suppresses the mTORC1 pathway. A Western blot results showed that overexpression of circEXOC6B suppressed the mTORC1 pathway. B Knockdown of circEXOC6B activated the mTORC1 pathway. C IHC indicated that p-mTOR and HIF1A expression was upregulated in the subcutaneous tumors with stable silencing of circEXOC6B expression. Scale: 20 μm. D Western blot results showed that the p-mTOR, p-S6K, and HIF1A elevation caused by RRAGB could be reversed by co-transfection with circEXOC6B. E EdU, F CCK8, G Colony formation assays showed that the enhanced proliferation and clonogenicity of CRC cells induced by RRAGB could be rescued by overexpression of circEXOC6B. Scale: 50 μm