Staufen1 controls mitochondrial metabolism via HIF2α in embryonal rhabdomyosarcoma and promotes tumorigenesis.


Journal

Cellular and molecular life sciences : CMLS
ISSN: 1420-9071
Titre abrégé: Cell Mol Life Sci
Pays: Switzerland
ID NLM: 9705402

Informations de publication

Date de publication:
17 Oct 2023
Historique:
received: 20 05 2023
accepted: 18 09 2023
revised: 31 08 2023
medline: 23 10 2023
pubmed: 17 10 2023
entrez: 17 10 2023
Statut: epublish

Résumé

Elevated mitochondrial metabolism promotes tumorigenesis of Embryonal Rhabdomyosarcomas (ERMS). Accordingly, targeting oxidative phosphorylation (OXPHOS) could represent a therapeutic strategy for ERMS. We previously demonstrated that genetic reduction of Staufen1 (STAU1) levels results in the inhibition of ERMS tumorigenicity. Here, we examined STAU1-mediated mechanisms in ERMS and focused on its potential involvement in regulating OXPHOS. We report the novel and differential role of STAU1 in mitochondrial metabolism in cancerous versus non-malignant skeletal muscle cells (NMSkMCs). Specifically, our data show that STAU1 depletion reduces OXPHOS and inhibits proliferation of ERMS cells. Our findings further reveal the binding of STAU1 to several OXPHOS mRNAs which affects their stability. Indeed, STAU1 depletion reduced the stability of OXPHOS mRNAs, causing inhibition of mitochondrial metabolism. In parallel, STAU1 depletion impacted negatively the HIF2α pathway which further modulates mitochondrial metabolism. Exogenous expression of HIF2α in STAU1-depleted cells reversed the mitochondrial inhibition and induced cell proliferation. However, opposite effects were observed in NMSkMCs. Altogether, these findings revealed the impact of STAU1 in the regulation of mitochondrial OXPHOS in cancer cells as well as its differential role in NMSkMCs. Overall, our results highlight the therapeutic potential of targeting STAU1 as a novel approach for inhibiting mitochondrial metabolism in ERMS.

Identifiants

pubmed: 37847286
doi: 10.1007/s00018-023-04969-4
pii: 10.1007/s00018-023-04969-4
doi:

Substances chimiques

Cytoskeletal Proteins 0
RNA, Messenger 0
STAU1 protein, human 0
RNA-Binding Proteins 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

328

Subventions

Organisme : Canadian Cancer Research Society
ID : 24303

Informations de copyright

© 2023. The Author(s), under exclusive licence to Springer Nature Switzerland AG.

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Auteurs

Shekoufeh Almasi (S)

Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.

Sahar SarmastiEmami (S)

Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.

Stephen Baird (S)

High Throughput Lab, CHEO, University of Ottawa, Ottawa, ON, K1H 8L1, Canada.

Zhibin Ning (Z)

School of Pharmaceutical Sciences, Faculty of Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.

Daniel Figeys (D)

School of Pharmaceutical Sciences, Faculty of Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.

Jocelyn Côté (J)

Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
The Eric J. Poulin Centre for Neuromuscular Diseases, Faculty of Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.

Kyle N Cowan (KN)

Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
Department of Surgery, Division of Paediatric Surgery, University of Ottawa, Children's Hospital of Eastern Ontario, Ottawa, ON, K1Y 4E9, Canada.
Molecular Biomedicine Program, Children's Hospital of Eastern Ontario, Ottawa, ON, K1H 8L1, Canada.

Bernard J Jasmin (BJ)

Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada. jasmin@uottawa.ca.
The Eric J. Poulin Centre for Neuromuscular Diseases, Faculty of Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada. jasmin@uottawa.ca.

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