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. 2017 Jun 28;16:111. doi: 10.1186/s12943-017-0681-0

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© The Author(s). 2017

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. 7 — MRCCAT1 suppresses NPR3 to potentiate p38- MAPK signaling. a Western blot analysis of indicated proteins in MRCCAT1 overexpressed and control 786-O cells transfected with pLVX -NPR3. β-actin was used as an internal control. b Western blot analysis of indicated proteins in MRCCAT1 overexpressed and control Caki-1 cells transfected with pLVX -NPR3. β-actin was used as an internal control. c Left: Transwell assays in MRCCAT1 overexpressed and control 786-O cells treated with SB203580. Scale bar = 200 μm. Right: The statistical graph indicates the number of cells averaged from 8 random high power fields. The results are presented as the mean ± SD from three independent experiments. P values were calculated by Student’s t-test