# Toronto team finds CSNK1 proximity degrades β-catenin in colorectal cancer cells in vitro

- Published: 2026-11-08 18:19 UTC
- Section: Life & Health › Biotechnology
- Tags: β-catenin degradation, Wnt pathway inhibition, Casein kinase I, induced-proximity drugs, colorectal cancer cells, neo-degron, genome-scale screen, E3 ubiquitin ligase, proteasome-dependent degradation
- URL: https://realtech.media/news/rt-24fa36f1a7f628daed546104_toronto_team_finds/

**A genome-scale screen at the University of Toronto found that bringing Casein kinase I close to β-catenin triggers its degradation and slows growth of colorectal cancer cells with Wnt mutations.**

![Toronto team finds CSNK1 proximity degrades β-catenin in colorectal cancer cells in vitro](https://realtech.media/media/2026/11/b826ec34b30c96f0.jpg)
*Diane A. Reid (Photographer), Wikimedia Commons, Public domain*

Researchers at the Donnelly Centre for Cellular and Biomolecular Research, University of Toronto, reported a genome-scale screen for proteins whose induced proximity to β-catenin reduces its levels in colorectal cancer cells. The work, led by Lucie Wolf, Mikko Taipale and Stéphane Angers, was published on 7 November 2026 in Nature Communications [1]. The experiments were carried out in cultured cells.

## Wnt pathway and induced proximity

β-catenin is the central effector of Wnt signaling. According to the authors, therapeutic strategies that inhibit this pathway in cancer have so far failed to advance to the clinic [1]. Induced-proximity drugs, which bring a target close to a protein that alters its fate, are described as expanding the range of targets previously considered undruggable [1].

The team used an unbiased genome-scale approach to look for candidate proteins that, when brought near β-catenin, inhibit it in colorectal cancer cells [1]. Several E3 ubiquitin ligases were among the hits, which the authors consider a validation of the approach [1].

## Casein kinase I and β-catenin degradation

The screen also showed that inducing proximity to members of the Casein kinase I (CSNK1) family leads to β-catenin degradation [1]. This inhibited the growth of colorectal cancer cells that carry Wnt pathway mutations [1].

The authors report that degradation induced by CSNK1 proximity depends on kinase activity and on the proteasome [1]. In other words, the enzymatic function of the recruited kinase and the cell's proteasomal machinery are both required for the effect.

The authors propose that recruiting a kinase can form a neo-degron, a new degradation signal on the target, and that this can broaden the targeting strategies available to induced-proximity drugs [1]. The material does not describe tests in animals or in patients; the results relate to cell-based experiments.

The study is open access under a CC BY-NC-ND 4.0 licence. Funding came from the Deutsche Forschungsgemeinschaft, the Charles H. Best Postdoctoral Fellowship and the Canadian Institutes of Health Research.

## Sources

1. [Nature Communications](https://doi.org/10.1038/s41467-026-79309-8)

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Source: RealTech, realtech.media — https://realtech.media/news/rt-24fa36f1a7f628daed546104_toronto_team_finds/