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. 2016 Sep 5;16:67. doi: 10.1186/s12935-016-0342-1

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© The Author(s) 2016

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. 6 — Expression of EMT markers when miR-23a is overexpressed in HEC-1-A cells. This experiment was conducted using treatment with 10 ng/mL TGFβ1 for 24 h, and the cells were then treated with the miR-23a agomir or antagomir investigate the effect of miR-23a on the EEC EMT. Non-treatment of TGFβ1 was used as the control group, and each group contained three samples. a, b Protein expression levels of the EMT markers. E-cadherin protein expression was increased when the HEC-1-A cells were treated with the miR-23a agomir but decreased when the cells were treated with the miR-23a antagomir. In contrast, the expression of both α-SMA and vimentin was decreased when the HEC-1-A cells were treated with the miR-23a agomir but increased when the cells were treated with the miR-23a antagomir. Top the gels (a); bottom the normalization graphs (b). c Up-regulation of miR-23a repressed the mRNA expression of EMT markers. The expression of mRNAs encoding α-SMA and vimentin was reduced in HEC-1-A cells treated with the miR-23a agomir but increased in cells treated with the miR-23a antagomir. However, the expression of E-cadherin mRNA was increased by the miR-23a agomir and decreased by the antagomir (n = 6 per group) (*P < 0.05)