Activation of the cGAS/STING axis in genome-damaged hematopoietic cells doesnNot impact blood cell formation or leukemogenesis
Genome damage is a main driver of malignant transformation, but it also induces aberrant inflammation via the cGAS/STING DNA-sensing pathway. Activation of cGAS/STING can trigger cell death and senescence, thereby potentially eliminating genome-damaged cells and preventing against malignant transfor...
Gespeichert in:
| Hauptverfasser: | , , , , , , , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
1 September 2023
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| In: |
Cancer research
Year: 2023, Jahrgang: 83, Heft: 17, Pages: 2858-2872 |
| ISSN: | 1538-7445 |
| DOI: | 10.1158/0008-5472.CAN-22-3860 |
| Online-Zugang: | Verlag, kostenfrei, Volltext: https://doi.org/10.1158/0008-5472.CAN-22-3860
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| Verfasserangaben: | Nicole Dressel, Loreen Natusch, Clara M. Munz, Santiago Costas Ramon, Mina N.F. Morcos, Anja Loff, Björn Hiller, Christa Haase, Livia Schulze, Patrick Müller, Mathias Lesche, Andreas Dahl, Hella Luksch, Angela Rösen-Wolff, Axel Roers, Rayk Behrendt, and Alexander Gerbaulet |
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| 245 | 1 | 0 | |a Activation of the cGAS/STING axis in genome-damaged hematopoietic cells doesnNot impact blood cell formation or leukemogenesis |c Nicole Dressel, Loreen Natusch, Clara M. Munz, Santiago Costas Ramon, Mina N.F. Morcos, Anja Loff, Björn Hiller, Christa Haase, Livia Schulze, Patrick Müller, Mathias Lesche, Andreas Dahl, Hella Luksch, Angela Rösen-Wolff, Axel Roers, Rayk Behrendt, and Alexander Gerbaulet |
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| 520 | |a Genome damage is a main driver of malignant transformation, but it also induces aberrant inflammation via the cGAS/STING DNA-sensing pathway. Activation of cGAS/STING can trigger cell death and senescence, thereby potentially eliminating genome-damaged cells and preventing against malignant transformation. Here, we report that defective ribonucleotide excision repair (RER) in the hematopoietic system caused genome instability with concomitant activation of the cGAS/STING axis and compromised hematopoietic stem cell function, ultimately resulting in leukemogenesis. Additional inactivation of cGAS, STING, or type I IFN signaling, however, had no detectable effect on blood cell generation and leukemia development in RER-deficient hematopoietic cells. In wild-type mice, hematopoiesis under steady-state conditions and in response to genome damage was not affected by loss of cGAS. Together, these data challenge a role of the cGAS/STING pathway in protecting the hematopoietic system against DNA damage and leukemic transformation.Loss of cGAS/STING signaling does not impact DNA damage-driven leukemogenesis or alter steady-state, perturbed or malignant hematopoiesis, indicating that the cGAS/STING axis is not a crucial antioncogenic mechanism in the hematopoietic system.See related commentary by Zierhut, p. 2807 | ||
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