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. 2022 Feb 21;41:71. doi: 10.1186/s13046-021-02237-6

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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. 8 — Clinical implication of circCUL2/miR-203a-3p/IL6 axis in PDAC. A, F, K The relative expression of miR-203a-3p (A), MyD88 (F) and IL6 (G) in 161 PDAC tissues compared to paired NAT. B-C, G-H, L-M Association analysis between miR-203a-3p (B-C), MyD88 (G-H) and IL6 (L-M) expression levels and LN status and tumor stages in 161 PDAC tissues. (D-E, I-J, N-O) Kaplan-Meier analysis of the correlation between miR-203a-3p (D-E), MyD88 (I-J) and IL6 (N-O) expression levels and OS or DFS of 161 PDAC patients. The median miR-203a-3p, MyD88 and IL6 expression was used as the cutoff value. P Proposed model indicates the mechanism by which circCUL2 activated iCAF phenotype and production of IL6 to promote malignant progression of PDAC via miR-203a-3p/MyD88/NF-κB pathway. Data are expressed as the mean ± SD. ^*p < 0.05 and ^***p < 0.001