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. 2015 Sep 23;15:645. doi: 10.1186/s12885-015-1655-5

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© Feng et al. 2015

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 4 — Verification of PDCD10 as a target of miR-200c. a. The binding sites of PDCD10 and TCF2-to miR-200c, and mFOLD analysis of free energy. b. Histogram of dual luciferase assay (a, compared with test group, P < 0.05). c. Experimental data of dual luciferase assay (a, compared with control groups, P < 0.05). d. In western blot assay, compared with empty vector (EV), Lenti-PDCD10 dramatically increases PDCD10 expression in BCSCs, and compared with miRNA control (miR-con), miR-200c agomir (miR-ag) dramatically decreases PDCD10 expression in BCSCs and MaSCs. e. In the 3-D matrigel culture, miR-200c agomir decreases, and Lenti-PDCD10 increases mammospheres of BCSCs compared with miR-control (P < 0.01, n = 5). Lenti-PDCD10 rescues mammospheres inhibited by miR-200c agomir (P < 0.01, n = 5)