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. 2022 May 7;21:110. doi: 10.1186/s12943-022-01586-w

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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 — Schematic diagram illustrates the mechanism of circHMGB2 relieves the inhibition of the downstream molecule CARM1 by sponging miR-181a-5p, which induces a reduction in the HDAC3 levels. Then, STAT1 deacetylation is inhibited, thereby reducing the phosphorylation of STAT1 and inhibiting IFN-γ signal transduction. Subsequently, the expression of IFN-activated genes, including CXCL10, ISG15, IL18, IFIT1, CCL5 and IFR7, were inhibited. Those drive immunosuppression and anti-PD-1 resistance in lung adenocarcinomas and squamous cell carcinomas