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. 2022 Jan 19;21:24. doi: 10.1186/s12943-022-01501-3

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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. 2 — circFARP1 is critical for CAFs to induce GEM resistance in PDAC cells. Panc-1 and MiaPaCa-2 cells were grown in conditioned medium (CM) from CAFs stably transfected with empty vector, circFARP1, lenti-NC-shRNA, or lenti-circFARP1-shRNA for 2 weeks and then subjected to the indicated experiments. A-B GEM IC50 of Panc-1 and MiaPaCa-2 determined by constructing a dose–response curve. C-D Cell proliferation of Panc-1 and MiaPaCa-2 cells was detected by CCK-8 assay with the indicated treatment. E-F Colony formation assays of Panc-1 and MiaPaCa-2 cells under GEM treatment (5 μM). G-H Spheroid growth assay of Panc-1 and MiaPaCa-2 cells under GEM treatment (5 μM). Scale bars, 50 μm. I-J Flow cytometry analysis of GEM-induced (10 μM) apoptosis in Panc-1 and MiaPaCa-2 cells. Data are expressed as the mean ± SD. **p<0.01 and ***p<0.001