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. 2024 Jun 25;150(6):319. doi: 10.1007/s00432-024-05845-9

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© The Author(s) 2024

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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Fig. 6 — MEX3A regulates CRC cell EMT transition and Wnt signal pathway. (A, B) β-catenin, c-Myc and phosphorylation β-catenin were decreased after the knockdown of MEX3A in HT29 and SW480 cell lines. (C) The β-catenin, phosphorylation β-catenin and c-Myc were increased when MEX3A was overexpressed in HCT116. (D, E) The β-catenin in the nucleus was decreased after the knockdown of MEX3A. (F, G)N-cadherin and Vimentin were decreased, and E-cadherin was increased after the knockdown of MEX3A in HT29 and SW480 cells. (H) N-cadherin and Vimentin were increased, and E-cadherin decreased in MEX3A-overexpressing HCT116 cells. (I) Immunofluorescence showed N-cadherin and E-cadherin changes with knockdown of MEX3A in HT29 cells