Copper – a novel stimulator of autophagy
Authors:Hans Zischka1,2 and Guido Kroemer3-7
1 Institute of Molecular Toxicology and Pharmacology, Helmholtz Center Munich, German Research Center for Environmental Health, Ingolstaedter Landstrasse 1, 85764 Neuherberg, Germany.
2 Technical University Munich, School of Medicine, Institute of Toxicology and Environmental Hygiene, Biedersteiner Strasse 29, 80802 Munich, Germany.
3 Centre de Recherche des Cordeliers, Equipe labellisée par la Ligue contre le cancer, Université de Paris, Sorbonne Université, Inserm U1138, Institut Universitaire de France, Paris, France.
4 Metabolomics and Cell Biology Platforms, Institut Gustave Roussy, Villejuif, France.
5 Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, Paris, France.
6 Suzhou Institute for Systems Medicine, Chinese Academy of Medical Sciences, Suzhou, China.
7 Karolinska Institute, Department of Women’s and Children’s Health, Karolinska University Hospital, Stockholm, Sweden.
Keywords:
autophagy, Wilson disease, copper, cancer, ULK1, ULK2, MEK1.
Corresponding Author(s):
Conflict of interest statement:
I am not aware of any possible conflict of interest.
Please cite this article as:
Hans Zischka and Guido Kroemer (2020). Copper – a novel stimulator of autophagy. Cell Stress 4(5): 92-94. doi: 10.15698/cst2020.05.218
© 2020 Zischka and Kroemer. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduc-tion in any medium, provided the original author and source are acknowledged.
Abstract:
Toxic copper accumulation causes Wilson disease, but trace amounts of copper are required for cellular and organismal survival. In a recent paper Tsang et al. (Nat Cell Biol, doi: 10.1038/s41556-020-0481-4) demonstrate that copper binds with high affinity to a designated interaction site in the pro-autophagic kinases ULK1 and ULK2. Chelation of copper or genetic deletion of this copper-binding site inhibits autophagy and hence reduces the fitness of KRAS-induced cancers. These findings suggest that copper chelation might constitute a novel therapeutic intervention on autophagy-dependent malignancies.