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. 2020 Oct 29;11(10):931. doi: 10.1038/s41419-020-03132-2

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© The Author(s) 2020

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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Fig. 6 — a HaCaT cells were transfected with RNA inhibitors as indicated and allowed to grow to confluent. E-cadherin protein was shown by immunofluorescence staining (green). Inhibition of miR-200b/c-3p led to dissociation of adherens junction as shown by loss of E-cadherin indicated by immunofluorescence average integrated optical intensity (IOD) (n = 12). b HaCaT cells transfected with RNA duplexes as indicated were fixed at 24 h post TGF-β1 treatment. Overexpression of miR-200b/c-3p or repression of RAC1 maintained the expression of E-cadherin (n = 12). c HaCaT cells were transfected with RNA duplexes as indicated and confluent cells were scratch wounded and treated with TGF-β1 for 24 h. Wound edge cells loss E-cadherin. Overexpression of miR-200b/c-3p or repression of RAC1 maintained the expression of E-cadherin (n = 12). Data presented as mean ± SD. **P < 0.01 versus negative control, one-way ANOVA. Scale bars: 25 μm.