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. 2020 Jul 17;146(10):2559–2574. doi: 10.1007/s00432-020-03317-4

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© The Author(s) 2020

Open AccessThis 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. 1 — Canonical Wnt signaling pathway: In absence of Wnt ligand (left), the destruction complex, consisting of GSK-3β, adenomatous polyposis coli (APC) and axin, hyperphosphorylates β-catenin, which marks it for ubiquitination (Ub) and proteasomal degradation. Binding of Wnt ligand (right) to a frizzled (FZD)/lipoprotein receptor-related protein (LRP) receptor complex leads to the phosphorylation of dishevelled (Dsh) inactivating GSK-3β and preventing the phosphorylation of β-catenin. Non-phosphorylated β-catenin shifts into the nucleus and forms a complex with T-cell factor (TCF)/lymphoid enhancer factor (LEF) activating transcription of Wnt target genes. Furthermore, the expression of zinc-finger transcription factors snail and slug is upregulated. They bind to E-boxes in E-cadherins promoter region and prevent its transcription. Suppresion of E-cadherin offers more available cytoplasmic β-catenin and induces a self-driven positive feedback loop. In conclusion, by losing E-cadherin as an adhesion molecule cells undergo EMT (Arend et al. 2013; Gasior et al. 2017; Gatcliffe et al. 2008). The three inhibitors (SB216763, XAV939 triptolide) used in this study, are shown in their typical domain