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. 2022 Apr 11;21:99. doi: 10.1186/s12943-021-01434-3

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© The Author(s) 2022

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/. 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 in a credit line to the data.

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Fig. 6 — PROTACs targeting cancer metastasis. Activation of Integrin/FAK/PI3K/AKT, TGF-β/SMAD and Wnt/β-catenin pathways significantly increase the expression of pro-EMT transcription factors (e.g. ZEB, SNAIL and TWIST), leading to the downregulation of E-cadherin (E-Cad) that maintains epithelial integrity, and the upregulation of N-cadherin (N-Cad) and vimentin (VIM) that implicate in motility and invasion. These key elements involved in metastasis can be targeted by PROTACs (red arrow). Tumor-suppressor proteins are indicated in blue and oncogenic proteins are indicated in red. In the presented pathways, PROTACs have been developed targeting FAK [246, 247], IGF-1R [248], p38 [249, 250], Smad3 [251], Src [248, 252], TCF [253], TGF-β1 [254] and β-catenin [255]