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. 2019 May 16;9:7504. doi: 10.1038/s41598-019-43668-8

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© The Author(s) 2019

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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CRAd regulates cancer cell migration through EMT reversal: Breast cancer cells (MCF-7 and M-231) and their resistant sublines (MCF-7/R and M-231/R) were treated with CRAd for 48 hr at an MOI of 5 and subsequently lysed and treated for protein expression analysis via blotting. (a,b) Western blot analysis shows that CRAd treatment (+) represses mesenchymal markers, vimentin and N-cadherin, while restores epithelial marker, E-cadherin expression. Controls (un-treated cells) showed opposite trends. The data shown above are the average of triplicate experiments (p < 0.05) and blot images were cropped for clarity of the presentation. (c–f) qRT-PCR detection of mRNA levels of EMT markers in human breast cancer cell lines upon CRAd treatment. The grouped blots were cropped from different parts of the same gel. Uncropped blots are shown in the Supplementary Information (See Supplementary Data, Figs S1 and S2).