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. 2021 Oct 18;40(47):6469–6478. doi: 10.1038/s41388-021-02059-y

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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 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. 2 — A Overexpression of RSPOs induces increased clearing of negative regulators ZNRF3/RNF43 from the membrane, thereby expanding membranous Wnt receptor availability and excessive activation of Wnt ligand-mediated pathway activation. B PORCN inhibitors block the availability of functional Wnt ligands, allowing the destruction complex to form and degrade β-catenin, resulting in inhibition of the Wnt pathway. Indicated PORCNi are tested in clinical trials for solid cancers considering the RSPO status. C Monoclonal anti-RSPO antibodies disable RSPOs to clear negative regulators ZNRF3/RNF43 from the membrane, causing ubiquitination and membrane clearance of Wnt receptors, as such inhibiting Wnt ligands to activate the pathway. Indicated antibody has been tested in a clinical trial for colorectal cancer.