Hypoxia Regulates Endogenous Double-Stranded RNA Production

IFN cancer dsRNA hypoxia mitochondria

Journal

Frontiers in oncology
ISSN: 2234-943X
Titre abrégé: Front Oncol
Pays: Switzerland
ID NLM: 101568867

Informations de publication

Date de publication:
2021
Historique:
received: 19 09 2021
accepted: 05 11 2021
entrez: 13 12 2021
pubmed: 14 12 2021
medline: 14 12 2021
Statut: epublish

Résumé

Hypoxia is a common phenomenon in solid tumours strongly linked to the hallmarks of cancer. Hypoxia promotes local immunosuppression and downregulates type I interferon (IFN) expression and signalling, which contribute to the success of many cancer therapies. Double-stranded RNA (dsRNA), transiently generated during mitochondrial transcription, endogenously activates the type I IFN pathway. We report the effects of hypoxia on the generation of mitochondrial dsRNA (mtdsRNA) in breast cancer. We found a significant decrease in dsRNA production in different cell lines under hypoxia. This effect was HIF1α/2α-independent. mtdsRNA was responsible for induction of type I IFN and significantly decreased after hypoxia. Mitochondrially encoded gene expression was downregulated and mtdsRNA bound by the dsRNA-specific J2 antibody was decreased during hypoxia. These findings reveal a new mechanism of hypoxia-induced immunosuppression that could be targeted by hypoxia-activated therapies.

Identifiants

pubmed: 34900733
doi: 10.3389/fonc.2021.779739
pmc: PMC8651540
doi:

Types de publication

Journal Article

Langues

eng

Pagination

779739

Subventions

Organisme : Cancer Research UK
ID : 11359
Pays : United Kingdom

Informations de copyright

Copyright © 2021 Arnaiz, Miar, Dias Junior, Prasad, Schulze, Waithe, Nathan, Rehwinkel and Harris.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Esther Arnaiz (E)

Department of Medical Oncology, Molecular Oncology Laboratories, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom.
Cambridge Institute for Therapeutic Immunology & Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, United Kingdom.

Ana Miar (A)

Department of Medical Oncology, Molecular Oncology Laboratories, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom.
Department of Oncology, Old Road Campus Research Building, University of Oxford, Oxford, United Kingdom.

Antonio Gregorio Dias Junior (AG)

Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.

Naveen Prasad (N)

Department of Oncology, Old Road Campus Research Building, University of Oxford, Oxford, United Kingdom.

Ulrike Schulze (U)

Radcliffe Department of Medicine, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom.

Dominic Waithe (D)

Radcliffe Department of Medicine, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom.

James A Nathan (JA)

Cambridge Institute for Therapeutic Immunology & Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, United Kingdom.

Jan Rehwinkel (J)

Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.

Adrian L Harris (AL)

Department of Medical Oncology, Molecular Oncology Laboratories, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom.

Classifications MeSH