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. 2022 Apr 23;8:223. doi: 10.1038/s41420-022-00919-4

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© The Author(s) 2022

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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Fig. 4 — A miR-17-5p expression in CRC tissues and adjacent normal tissues detected using RT-qPCR (n = 70); B proliferation of HCT116 cells detected using colony-formation assay after treated with CRCSC-exos transmitting miR-17-5p mimic/inhibitor; C proliferation of HCT116 cells detected using CCK-8 assay after treated with CRCSC-exos transmitting miR-17-5p mimic/inhibitor; D apoptosis of HCT116 cells detected using flow cytometry after treated with CRCSC-exos transmitting miR-17-5p mimic/inhibitor; E migration and invasion of HCT116 cells detected using Transwell assay after treated with CRCSC-exos transmitting miR-17-5p mimic/inhibitor. The cell experiments were repeated three times; *P < 0.05 vs the miR-17-5p-NC-Exo group; the measurement data were expressed as mean ± standard deviation.