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. 2018 Jan 10;8:327. doi: 10.1038/s41598-017-18612-3

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© The Author(s) 2017

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/.

PMC Copyright notice

MiR655 expression results in TGFβ resistance. (A) Both MCF7-miR655 and MCF7-COX2 cells show significantly high expression of TGFβR2 and high expression of COX-2 mRNA compared to MCF7 cells. We treated all three cell lines with TGFβ1 (5 ng/ml) and collected cell lysates at various time intervals 0, 8, 12 and 24 hrs and measured pSmad3 with InstantOne™ ELISA. Phosphorylated SMAD3 (Ser423/425) was measured in cell lysates by absorption values at 450 nm. (B) pSmad3 was significantly upregulated in MCF7; (C) but no change was noted in MCF7-miR655 cells. (D) MCF7 cell morphology changed with TGF-β1 treatment from epitheloid to fibroblast-like, however MCF7-miR655 cell morphology (fibroblast-like) did not change. (E) Schema represents possible regulation of miR655 by COX-2 and vice-versa.