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. 2018 Jun 7;9(6):680. doi: 10.1038/s41419-018-0738-z

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© The Author(s) 2018

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. 2 — a Cell proliferation was evaluated by the CCK-8 assay at 24, 48 and 72 h. b The effects of miR-16-5p on the cell cycle were determined by flow cytometry (FCM). c FCM indicated G0/G1-phase arrest of the cell cycle in cells transfected with miR-16-5p mimics. d Tumor volume was significantly decreased in the miR-16-5p agomir treatment group compared with the control group. e Representative images of H&E staining of tumors formed by U-CH1 cells. f qRT-PCR results showing that miR-16-5p was significantly upregulated in the miR-16-5p agomir treatment group compared with the control group. g The tumor volume was measured every 7 days, and the growth curves of the tumors were plotted accordingly. **p < 0.01.