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Type: Journal article
Title: The tumor-modulatory effects of Caspase-2 and Pidd1 do not require the scaffold protein Raidd
Author: Peintner, L.
Dorstyn, L.
Kumar, S.
Aneichyk, T.
Villunger, A.
Manzl, C.
Citation: Cell Death and Differentiation, 2015; 22(11):1803-1811
Publisher: Nature
Issue Date: 2015
ISSN: 1350-9047
Statement of
L Peintner, L Dorstyn, S Kumar, T Aneichyk, A Villunger, and C Manzl
Abstract: The receptor-interacting protein-associated ICH-1/CED-3 homologous protein with a death domain (RAIDD/CRADD) functions as a dual adaptor and is a constituent of different multi-protein complexes implicated in the regulation of inflammation and cell death. Within the PIDDosome complex, RAIDD connects the cell death-related protease, Caspase-2, with the p53-induced protein with a death domain 1 (PIDD1). As such, RAIDD has been implicated in DNA-damage-induced apoptosis as well as in tumorigenesis. As loss of Caspase-2 leads to an acceleration of tumor onset in the Eμ-Myc mouse lymphoma model, whereas loss of Pidd1 actually delays onset of this disease, we set out to interrogate the role of Raidd in cancer in more detail. Our data obtained analyzing Eμ-Myc/Raidd(-/-) mice indicate that Raidd is unable to protect from c-Myc-driven lymphomagenesis. Similarly, we failed to observe a modulatory effect of Raidd deficiency on DNA-damage-driven cancer. The role of Caspase-2 as a tumor suppressor and that of Pidd1 as a tumor promoter can therefore be uncoupled from their ability to interact with the Raidd scaffold, pointing toward the existence of alternative signaling modules engaging these two proteins in this context.
Keywords: Cells, Cultured
DNA Damage
Proto-Oncogene Proteins c-myc
Cell Cycle
Cell Survival
Caspase 2
Death Domain Receptor Signaling Adaptor Proteins
CRADD Signaling Adaptor Protein
Rights: This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit © 2015 Macmillan Publishers Limited
DOI: 10.1038/cdd.2015.31
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