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. 2021 Apr 14;11:8091. doi: 10.1038/s41598-021-87525-z

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© The Author(s) 2021

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Combination of M + P affects EMT in CRC cells. (A,B) The migratory ability of HCT116 cells was estimated by measuring closure of the initial wound. Pictures were taken (A) to allow quantification of healing (B) by using the Image J software (AUC, area under the curve). (C) Focal adhesions were highlighted by Immunofluorescent detection of vinculin (green color, left panel) and FAK (green color, middle panel) in HCT116 cells counterstained with F-actin and nuclei (red and blue colors respectively, scale bar = 10 µm) and quantified (right panel). (D) Representative immunoblots showing modulation of EMT markers expression by M + P treatment. For loading control, we used the abundance of endogenous tubulin (n = 3 independent experiments). (E) Representative immunofluorescence analysis showing the abundance and subcellular localization of endogenous E-cadherin (green color, left panel), β-catenin (green color, right panel), rhodamine phalloidin-stained F-actin (red color), and DAPI-stained nuclei (blue color). Arrows indicate increased detection at cellular junctions (scale bar = 10 µm).