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. 2022 Jan 4;21:10. doi: 10.1186/s12943-021-01481-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. 1 — circRTN4 is upregulated in PDAC cells and primary tumors and associates with liver metastasis. A CircRTN4 was upregulated in a panel of PDAC cells, compared to non-tumor HPDE cells. B CircRTN4 was significantly upregulated in PDAC primary tumors, compared to respective adjacent non-tumor tissues (n = 88). CircRTN4 was upregulated in 60% of the PDAC primary tumors (53 out of 88), while 18% of PDAC patients showed downregulated circRTN4 (16 out of 88), and 22% of PDAC patients showed unchanged circRTN4 (19 out of 88). C CircRTN4 was upregulated in PDAC primary tumors from patients with liver metastasis. D CircRTN4 was formed by back-splicing of exon 4 and 5 of RTN4 mRNA. Data represent mean ± SD from at least three independent experiments (*p < 0.05; **p < 0.01***p < 0.001)