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Non-canonical β-catenin degradation mediates reactive oxygen species-induced epidermal cell death

Abstract

β-Catenin is constantly degraded through the ubiquitin-proteasomal pathway. In this study, we report that a different type of β-catenin degradation is causally involved in epidermal cell death. We observed that reactive oxygen species (ROS) caused β-catenin degradation in the epidermal cells through a caspase-dependent mechanism, which results in disruption of cell adhesion. Disruption of cell adhesion increased ROS and activated caspases. Upregulation of the intact β-catenin blocked ROS accumulation and caspase activation. These results indicate that a feed-forward loop consisting of ROS, caspases activation and β-catenin degradation induces epidermal cell death.

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Acknowledgements

We thank S Akira for tak1-floxed mice, ER Fearon for β-catenin cDNAs, J Dow, BJ Welker and M Mattmuler for support. This work was supported by National Institutes of Health Grant GM068812 and GM084406 (to J N-T).

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Correspondence to J Ninomiya-Tsuji.

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Supplementary Information accompanies the paper on the Oncogene website ()

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Omori, E., Matsumoto, K. & Ninomiya-Tsuji, J. Non-canonical β-catenin degradation mediates reactive oxygen species-induced epidermal cell death. Oncogene 30, 3336–3344 (2011). https://doi.org/10.1038/onc.2011.49

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