Glutamine and serum starvation alters the ATP production, oxidative stress, and abundance of mitochondrial RNAs in extracellular vesicles produced by cancer cells.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
28 10 2024
Historique:
received: 15 04 2024
accepted: 23 09 2024
medline: 29 10 2024
pubmed: 29 10 2024
entrez: 29 10 2024
Statut: epublish

Résumé

Induction of autophagy represents an effective survival strategy for nutrient-deprived or stressed cancer cells. Autophagy contributes to the modulation of communication within the tumor microenvironment. Here, we conducted a study of the metabolic and signaling implications associated with autophagy induced by glutamine (Gln) and serum starvation and PI3K/mTOR inhibitor and autophagy inducer NVP-BEZ235 (BEZ) in the head and neck squamous cell carcinoma (HNSCC) cell line FaDu. We compared the effect of these different types of autophagy induction on ATP production, lipid peroxidation, mitophagy, RNA cargo of extracellular vesicles (EVs), and EVs-associated cytokine secretome of cancer cells. Both BEZ and starvation resulted in a decline in ATP production. Simultaneously, Gln starvation enhanced oxidative damage of cancer cells by lipid peroxidation. In starved cells, there was a discernible fragmentation of the mitochondrial network coupled with an increase in the presence of tumor susceptibility gene 101 (TSG101) on the mitochondrial membrane, indicative of the sorting of mitochondrial cargo into EVs. Consequently, the abundance of mitochondrial RNAs (mtRNAs) in EVs released by FaDu cells was enhanced. Notably, mtRNAs were also detectable in EVs isolated from the serum of both HNSCC patients and healthy controls. Starvation and BEZ reduced the production of EVs by cancer cells, yet the characteristic molecular profile of these EVs remained unchanged. We also found that alterations in the release of inflammatory cytokines constitute a principal response to autophagy induction. Importantly, the specific mechanism driving autophagy induction significantly influenced the composition of the EVs-associated cytokine secretome.

Identifiants

pubmed: 39468126
doi: 10.1038/s41598-024-73943-2
pii: 10.1038/s41598-024-73943-2
doi:

Substances chimiques

Adenosine Triphosphate 8L70Q75FXE
Glutamine 0RH81L854J
RNA, Mitochondrial 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

25815

Subventions

Organisme : Grantová Agentura České Republiky
ID : GACR-21-06873S
Organisme : Grantová Agentura České Republiky
ID : GACR-21-06873S
Organisme : Grantová Agentura České Republiky
ID : GACR-21-06873S
Organisme : Grantová Agentura České Republiky
ID : GACR-21-06873S
Organisme : Ministerstvo Zdravotnictví Ceské Republiky
ID : NU20J-08-00018
Organisme : Ministerstvo Zdravotnictví Ceské Republiky
ID : NU20J-08-00018
Organisme : Ministerstvo Zdravotnictví Ceské Republiky
ID : NU20J-08-00018
Organisme : Ministerstvo Zdravotnictví Ceské Republiky
ID : NU20J-08-00018
Organisme : Ministerstvo Zdravotnictví Ceské Republiky
ID : NU20J-08-00018
Organisme : Ministerstvo Zdravotnictví Ceské Republiky
ID : NU20J-08-00018

Informations de copyright

© 2024. The Author(s).

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Auteurs

Maria Bugajova (M)

Department of Pathological Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, Brno, CZ-625 00, Czech Republic.

Martina Raudenska (M)

Department of Pathological Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, Brno, CZ-625 00, Czech Republic.
Department of Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, Brno, CZ-625 00, Czech Republic.

Klara Hanelova (K)

Department of Pathological Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, Brno, CZ-625 00, Czech Republic.

Jiri Navratil (J)

Department of Pathological Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, Brno, CZ-625 00, Czech Republic.

Jaromir Gumulec (J)

Department of Pathological Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, Brno, CZ-625 00, Czech Republic.
Department of Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, Brno, CZ-625 00, Czech Republic.

Frantisek Petrlak (F)

Department of Chemistry and Biochemistry, Mendel University in Brno, Zemedelska 1, Brno, CZ-613 00, Czech Republic.

Tomas Vicar (T)

Department of Pathological Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, Brno, CZ-625 00, Czech Republic.

Sarka Hrachovinova (S)

Department of Experimental Biology, Faculty of Science, Masaryk University, Kamenice 5, Brno, CZ- 625 00, Czech Republic.

Michal Masarik (M)

Department of Pathological Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, Brno, CZ-625 00, Czech Republic.
Department of Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, Brno, CZ-625 00, Czech Republic.
First Faculty of Medicine, BIOCEV, Charles University, Prumyslova 595, Vestec, CZ-252 50, Czech Republic.

David Kalfert (D)

Department of Otorhinolaryngology and Head and Neck Surgery, First Faculty of Medicine, University Hospital Motol, Charles University, V Uvalu 84, Prague, CZ-15006, Czech Republic.

Marek Grega (M)

Department of Pathology and Molecular Medicine, 2nd Faculty of Medicine, Charles University, University Hospital Motol/ V Uvalu 84, Prague 5, CZ-15006, Czech Republic.

Jan Plzak (J)

Department of Otorhinolaryngology and Head and Neck Surgery, First Faculty of Medicine, University Hospital Motol, Charles University, V Uvalu 84, Prague, CZ-15006, Czech Republic.

Jan Betka (J)

Department of Otorhinolaryngology and Head and Neck Surgery, First Faculty of Medicine, University Hospital Motol, Charles University, V Uvalu 84, Prague, CZ-15006, Czech Republic.

Jan Balvan (J)

Department of Pathological Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, Brno, CZ-625 00, Czech Republic. jan.balvan@med.muni.cz.

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