Small-molecule inhibition of Wnt signaling through activation of casein kinase 1α
Open accessAbstract
Wnt/β-catenin signaling is critically involved in metazoan development, stem cell maintenance and human disease. Using Xenopus laevis egg extract to screen for compounds that both stabilize Axin and promote β-catenin turnover, we identified an FDA-approved drug, pyrvinium, as a potent inhibitor of Wnt signaling (EC(50) of ∼10 nM). We show pyrvinium binds all casein kinase 1 (CK1) family members in vitro at low nanomolar concentrations and pyrvinium selectively potentiates casein kinase 1α (CK1α) kinase activity. CK1α knockdown abrogates the effects of pyrvinium on the Wnt pathway. In addition to its effects on Axin and β-catenin levels, pyrvinium promotes degradation of Pygopus, a Wnt transcriptional component. Pyrvinium treatment of colon cancer cells with mutation of the gene for adenomatous polyposis coli (APC) or β-catenin inhibits both Wnt signaling and proliferation. Our findings reveal allosteric activation of CK1α as an effective mechanism to inhibit Wnt signaling and highlight a new strategy for targeted therapeutics directed against the Wnt pathway.
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Pyrvinium, which destabilizes β-catenin, reduced the number of BrdU-positive progenitors induced by HB-EGF.
“Pharmacological destabilization of β-catenin with pyrvinium (Thorne et al., 2010), dramatically reduced the number of HB-EGF induced BrdU+ progenitors (Figure 7C and 7D), and suppressed HB-EGF-dependent induction of regeneration-associated genes (Figure 7E).”
From HB-EGF is Necessary and Sufficient for Müller Glia Dedifferentiation and Retina Regeneration (2012) · cites this paper as Thorne et al., 2010
Pyrvinium suppressed HB-EGF-dependent induction of regeneration-associated genes.
“Pharmacological destabilization of β-catenin with pyrvinium (Thorne et al., 2010), dramatically reduced the number of HB-EGF induced BrdU+ progenitors (Figure 7C and 7D), and suppressed HB-EGF-dependent induction of regeneration-associated genes (Figure 7E).”
From HB-EGF is Necessary and Sufficient for Müller Glia Dedifferentiation and Retina Regeneration (2012) · cites this paper as Thorne et al., 2010
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“Pharmacological destabilization of β-catenin with pyrvinium (Thorne et al., 2010), dramatically reduced the number of HB-EGF induced BrdU+ progenitors (Figure 7C and 7D), and suppressed HB-EGF-dependent induction of regeneration-associated genes (Figure 7E).”
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- Authors
- Thorne, C. A., Hanson, A. J., Schneider, J., Tahinci, E., Orton, D., Cselenyi, C. S., Jernigan, K. K., Meyers, K. C., Hang, B. I., Waterson, A. G., Kim, K., Melancon, B., Ghidu, V. P., Sulikowski, G. A., LaFleur, B., Salic, A., Lee, L. A., Miller, D. M., & Lee, E.
- Affiliations
- Vanderbilt University Medical Center (US)
- Vanderbilt University (US)
- Harvard University (US)
- Corresponding author
- Lee, Ethan
- ORCID
- Venue
- Nature Chemical Biology
- Published
- 2010-10-03
- Volume
- 6
- Issue
- 11
- Pages
- 829-836
- ISSN
- 1552-4450 (ISSN-L)
- 1552-4469
- PMC
- PMC3681608
- OpenAlex
- W2034373020
- Cited by
- 485
- References
- 50
- Citations by year
- 2026: 20 · 2025: 23 · 2024: 24 · 2023: 30 · 2022: 28 · 2021: 33 · 2020: 36 · 2019: 32 · 2018: 26 · 2017: 32 · 2016: 28 · 2015: 37 · 2014: 41 · 2013: 31 · 2012: 39
- FWCI
- 12.54
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Chemical Biology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R33CA086243, P50CA095103, U01CA084239, T32CA009592, P30CA068485)
- National Institute of General Medical Sciences (R01GM081635, P50GM015431, T32GM007347)
- National Institute of Diabetes and Digestive and Kidney Diseases (T32DK007563, P30DK058404)
- National Institute of Neurological Disorders and Stroke (R01NS026115)
- National Institute of Environmental Health Sciences (P30ES000267)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (T32HD007502)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Hedgehog Signaling Pathway Studies
- Keywords
- Wnt/β-catenin signaling, CK1α, pyrvinium, antihelminthic drugs, small molecule inhibitors, colon cancer, APC mutation, drug repurposing
- MeSH terms
- Animals, Cell Extracts, Colonic Neoplasms, Dose-Response Relationship, Drug, Enzyme Activation, Enzyme Inhibitors, Humans, Oocytes, Adenomatous Polyposis Coli, Pyrvinium Compounds, Repressor Proteins, Xenopus laevis, Signal Transduction, Xenopus Proteins, Cell Line, Tumor, Casein Kinase I, Intracellular Signaling Peptides and Proteins, Casein Kinase Ialpha, Adaptor Proteins, Signal Transducing, Cell Proliferation, Wnt Proteins, beta Catenin, Axin Protein
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