Mitochondrial control of innate immune signaling by irradiated cancer cells

Type I interferon (IFN) release by irradiated cancer cells is paramount for radiation therapy to elicit anticancer immunity. Our findings demonstrate that mitochondrial outer membrane permeabilization (MOMP) triggered by RT enables exposure of mitochondrial DNA to the cytosol, hence setting off CGAS...

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Detalles Bibliográficos
Autores principales: Yamazaki, Takahiro, Galluzzi, Lorenzo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2020
Materias:
Editorial
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7458622/
https://www.ncbi.nlm.nih.gov/pubmed/32923160
http://dx.doi.org/10.1080/2162402X.2020.1797292
Descripción
Sumario:Type I interferon (IFN) release by irradiated cancer cells is paramount for radiation therapy to elicit anticancer immunity. Our findings demonstrate that mitochondrial outer membrane permeabilization (MOMP) triggered by RT enables exposure of mitochondrial DNA to the cytosol, hence setting off CGAS-driven type I IFN synthesis. These data point to the existence of a therapeutically actionable mitochondrial checkpoint that restricts innate immune signaling in irradiated cancer cells.

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