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Widespread non-apoptotic activation of Drosophila Caspase-2/9 limits JNK signaling, macrophage proliferation, and growth of wound-like tumors

View ORCID ProfileDerek Cui Xu, View ORCID ProfileKenneth M. Yamada, View ORCID ProfileLuis Alberto Baena-Lopez
doi: https://doi.org/10.1101/2020.07.27.223404
Derek Cui Xu
1Cell Biology Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4370, USA
2Sir William Dunn School of Pathology, University of Oxford, Oxford, Oxfordshire, OX1 3RE, UK
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Kenneth M. Yamada
1Cell Biology Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4370, USA
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  • For correspondence: kenneth.yamada@nih.gov alberto.baenalopez@path.ox.ac.uk
Luis Alberto Baena-Lopez
2Sir William Dunn School of Pathology, University of Oxford, Oxford, Oxfordshire, OX1 3RE, UK
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  • For correspondence: kenneth.yamada@nih.gov alberto.baenalopez@path.ox.ac.uk
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Summary

Resistance to apoptosis due to caspase deregulation is considered one of the main hallmarks of cancer. However, the discovery of novel non-apoptotic caspase functions has revealed unknown intricacies about the interplay between these enzymes and tumor progression. To investigate this biological problem, we capitalized on a Drosophila tumor model highly relevant for humans that relies on the concomitant upregulation of EGFR and the JAK/STAT signaling pathway. Our results indicate that widespread non-apoptotic activation of initiator caspases limits JNK signaling and facilitates cell fate commitment in these tumors, thus preventing the overgrowth and exacerbation of malignant features. Intriguingly, these caspase functions are strongly linked to the ability of these enzymes to control the recruitment and subsequent proliferation in situ of macrophage-like cells on the tumor. These findings assign novel tumor-suppressor activities to caspases independent of apoptosis, while providing highly relevant molecular details to understanding their diverse contribution during tumor progression.

Competing Interest Statement

The authors have declared no competing interest.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted July 27, 2020.
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Widespread non-apoptotic activation of Drosophila Caspase-2/9 limits JNK signaling, macrophage proliferation, and growth of wound-like tumors
Derek Cui Xu, Kenneth M. Yamada, Luis Alberto Baena-Lopez
bioRxiv 2020.07.27.223404; doi: https://doi.org/10.1101/2020.07.27.223404
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Widespread non-apoptotic activation of Drosophila Caspase-2/9 limits JNK signaling, macrophage proliferation, and growth of wound-like tumors
Derek Cui Xu, Kenneth M. Yamada, Luis Alberto Baena-Lopez
bioRxiv 2020.07.27.223404; doi: https://doi.org/10.1101/2020.07.27.223404

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