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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. 5 — circCCDC134 stimulates HIF1A transcription by recruiting p65. A The molecular simulation results supported that circCCDC134 could perfectly dock p65. The results of B: circRNA pull-down and C: RIP assays demonstrated that p65 could interact with circCCDC134, and D: no significant change was found in the p65 protein levels upon circCCDC134 knockdown. E Heatmaps and G: pie charts of p65 ChIP-seq. HIF1A was found to be the key target gene of p65. H and I p65 was enriched in the region − 1200 to − 400 bp from the transcription start site of the HIF1A promoter. p65 enrichment of the HIF1A promoter was reduced after interfering with J: p65 and K: circCCDC134 expression. L The expression of HIF1A was positively correlated with the expression of circCCDC134. M and N Immunohistochemistry showed that HIF1A was positively correlated with the expression of circCCDC134 in the xenograft growth and lung metastasis models