Research Papers:

Respiratory status determines the effect of emodin on cell viability

Verónica I. Dumit, Ralf M. Zerbes, Stephanie Kaeser-Pebernard, Michal Rackiewicz, Mona T. Wall, Christine Gretzmeier, Victoria Küttner, Martin van der Laan, Ralf J. Braun and Jörn Dengjel _

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Oncotarget. 2017; 8:37478-37490. https://doi.org/10.18632/oncotarget.16396

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Verónica I. Dumit1,2,3,4, Ralf M. Zerbes5,6, Stephanie Kaeser-Pebernard10, Michal Rackiewicz2,3,10, Mona T. Wall1,2, Christine Gretzmeier2,3, Victoria Küttner2,3, Martin van der Laan5,7,8, Ralf J. Braun9 and Jörn Dengjel1,2,3,7,10

1Freiburg Institute for Advanced Studies FRIAS, University of Freiburg, Freiburg, Germany

2Center for Biological Systems Analysis ZBSA, Freiburg, Germany

3Department of Dermatology, Medical Center, University of Freiburg, Freiburg, Germany

4Core Facility Proteomics, ZBSA, University of Freiburg, Freiburg, Germany

5Institute of Biochemistry and Molecular Biology, ZBMZ, Faculty of Medicine, University of Freiburg, Freiburg, Germany

6Faculty of Biology, University of Freiburg, Freiburg, Germany

7BIOSS Centre for Biological Signalling Studies, University of Freiburg, Freiburg, Germany

8Medical Biochemistry and Molecular Biology, Center for Molecular Signaling, PZMS, Saarland University, Homburg, Germany

9Institute of Cell Biology, University of Bayreuth, Bayreuth, Germany

10Department of Biology, University of Fribourg, Fribourg, Switzerland

Correspondence to:

Jörn Dengjel, email: [email protected]

Verónica I. Dumit, email: [email protected]

Keywords: chemoproteomics, reactive oxygen species, mitochondria, anthraquinone, complex I

Received: September 09, 2016    Accepted: March 01, 2017    Published: March 21, 2017


The anthraquinone emodin has been shown to have antineoplastic properties and a wealth of unconnected effects have been linked to its use, most of which are likely secondary outcomes of the drug treatment. The primary activity of emodin on cells has remained unknown. In the present study we demonstrate dramatic and extensive effects of emodin on the redox state of cells and on mitochondrial homeostasis, irrespectively of the cell type and organism, ranging from the yeast Saccharomyces cerevisiae to human cell lines and primary cells. Emodin binds to redox-active enzymes and its effectiveness depends on the oxidative and respiratory status of cells. We show that cells with efficient respiratory metabolism are less susceptible to emodin, whereas cells under glycolytic metabolism are more vulnerable to the compound. Our findings indicate that emodin acts in a similar way as known uncouplers of the mitochondrial electron transport chain and causes oxidative stress that particularly disturbs cancer cells.

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