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. 2020 Feb 21;10:3161. doi: 10.1038/s41598-020-59939-8

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© The Author(s) 2020

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Overexpression of miR-1229-3p induced chemoresistance to 5-FU in vivo. (a) Investigation into whether miR-1229-3p could induce chemoresistance in vivo. To evaluate the chemoresistant function of miR-1229-3p, intraperitoneal injection of miR-1229-3p with AteloGene or only AteloGene was repeated every 3 days for 2 weeks. Furthermore, 5-FU or PBS was injected into the intraperitoneal cavity on the day after the injection of the AteloGene with or without miR-1229-3p mimics. In addition to these two treatment groups, the result of non-treatment group was checked. (b) The miR-1229-3p mimic significantly induced chemoresistance to 5-FU compared with the control. Error bars indicate s.e.m; n = 4 mice per group. (c,d) Plasma and tumor miR-1229-3p levels were significantly higher in mice with miR-1229-3p mimics than only AteloGene. Error bars indicate s.e.m; n = 4 mice per group. (e) Tumor SLC22A7 level was lower in mice with miR-1229-3p than with only AteloGene. Moreover, tumor TS and DPD levels were significantly higher in mice with miR-1229-3p than with only AteloGene.