Colorectal cancer is one of the most common forms of cancer in the world, with more than half a million new cases annually. Amongst the most promising new therapies, niclosamide—an FDA-approved drug for treating tapeworm infections—is being assessed in a stage II clinical trial for the treatment of metastatic colorectal cancer. Despite this advanced stage of research, the underlying mechanisms behind its actions remain uncertain. Niclosamide reduces the growth of colorectal cancer cells by targeting several intracellular signalling pathways, including the β-catenin-dependent WNT signalling pathway. In a recent paper published in the Biochemical Journal [Biochem. J. (2019) 476, 535–546], Wang and colleagues revealed that niclosamide down-regulates β-catenin-dependent WNT signalling in colorectal cancer cells by degrading components of the pathway via autophagy. Autophagy is a catabolic process in which cellular macromolecules and organelles are recycled to their monomer units. This finding provides a further understanding of the actions of niclosamide upon colorectal cancer cells and may yield improved future treatment models for colorectal cancer patients.

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