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. 2018 Jan 25;37(15):1991–2007. doi: 10.1038/s41388-017-0081-3

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License, which permits any non-commercial 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. If you remix, transform, or build upon this article or a part thereof, you must distribute your contributions under the same license as the original. 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-nc-sa/4.0/.

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Fig. 7 — Oncogenic miR-486-5p contributes to FP-RMS pathogenesis. a Expression of miR-486-5p by qRT-PCR in patient-derived xenografts from the CSTN consisting of 13 FN-RMS and 4 FP-RMS samples. b Transwell migration and c invasion assays in Rh41 cells transfected with NC or antimiR-486-5p. d Clonogenic colony formation assay in Rh41 cells transfected with NC or antimiR-486-5p. ***P < 0.001, ****P < 0.0001 for FP-RMS vs FN-RMS or antimiR-486 vs NC antimiR