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. 2024 May 30;22:517. doi: 10.1186/s12967-024-05233-4

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© The Author(s) 2024

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. 1 — Selection and identification of circDCAF8. A The volcano plot of DECs in GSE94508. B A heatmap of the top 10 upregulated circRNAs in 5 paired samples of HCC. C Relative expression of circDCAF8 in human HCC tissues and paired adjacent nontumor tissues of 64 patients was determined by qRT-PCR. D Sanger sequencing of the annotated genomic region of circDCAF8 was performed to confirm the Back-spliced site of circDCAF8. E The divergent primers detected circDCAF8 in cDNA but not in gDNA by agarose gel electrophoresis. GAPDH was used as a negative control. F qRT–PCR analysis for the expression of circDCAF8 and mDCAF8 after treatment with RNase R in Hep-G2 and Hep-3B cells. Data are representative of three independent experiments and are presented as means ± SDs. (*p < 0.05; **p < 0.01; ***p < 0.001)