α-Ketoglutarate supplementation and NAD+ modulation enhance metabolic rewiring and radiosensitization in SLC25A1 inhibited cancer cells.


Journal

Cell death discovery
ISSN: 2058-7716
Titre abrégé: Cell Death Discov
Pays: United States
ID NLM: 101665035

Informations de publication

Date de publication:
15 Jan 2024
Historique:
received: 18 07 2023
accepted: 04 01 2024
revised: 22 12 2023
medline: 16 1 2024
pubmed: 16 1 2024
entrez: 15 1 2024
Statut: epublish

Résumé

Metabolic rewiring is the result of the increasing demands and proliferation of cancer cells, leading to changes in the biological activities and responses to treatment of cancer cells. The mitochondrial citrate transport protein SLC25A1 is involved in metabolic reprogramming offering a strategy to induce metabolic bottlenecks relevant to radiosensitization through the accumulation of the oncometabolite D-2-hydroxyglutarate (D-2HG) upon SLC25A1 inhibition (SLC25A1i). Previous studies have revealed the comparative effects of SLC25A1i or cell-permeable D-2HG (octyl-D-2HG) treatments on DNA damage induction and repair, as well as on energy metabolism and cellular function, which are crucial for the long-term survival of irradiated cells. Here, α-ketoglutarate (αKG), the precursor of D-2HG, potentiated the effects observed upon SLC25A1i on DNA damage repair, cell function and long-term survival in vitro and in vivo, rendering NCI-H460 cancer cells more vulnerable to ionizing radiation. However, αKG treatment alone had little effect on these phenotypes. In addition, supplementation with nicotinamide (NAM), a precursor of NAD (including NAD

Identifiants

pubmed: 38225236
doi: 10.1038/s41420-024-01805-x
pii: 10.1038/s41420-024-01805-x
doi:

Types de publication

Journal Article

Langues

eng

Pagination

27

Subventions

Organisme : Bundesministerium für Bildung und Forschung (Federal Ministry of Education and Research)
ID : 02NUK061B
Organisme : Deutsche Forschungsgemeinschaft (German Research Foundation)
ID : MA 8970/1-1
Organisme : Deutsche Forschungsgemeinschaft (German Research Foundation)
ID : GRK1739/2
Organisme : EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)
ID : 860245
Organisme : EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)
ID : 860245

Informations de copyright

© 2024. The Author(s).

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Auteurs

Kexu Xiang (K)

Institute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147, Essen, Germany.
Department of Gastroenterology, Chongqing University Cancer Hospital, 400030, Chongqing, China.
Chongqing Key Laboratory of Translational Research for Cancer Metastasis and Individualized Treatment, Chongqing University Cancer Hospital, 400030, Chongqing, China.

Mikhail Kunin (M)

Institute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147, Essen, Germany.

Safa Larafa (S)

Institute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147, Essen, Germany.

Maike Busch (M)

Center for Translational Neuro- and Behavioral Sciences, Institute of Anatomy II, Department of Neuroanatomy, Medical Faculty, University of Duisburg-Essen, 45147, Essen, Germany.

Nicole Dünker (N)

Center for Translational Neuro- and Behavioral Sciences, Institute of Anatomy II, Department of Neuroanatomy, Medical Faculty, University of Duisburg-Essen, 45147, Essen, Germany.

Verena Jendrossek (V)

Institute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147, Essen, Germany.
German Cancer Consortium (DKTK) partner site Essen a partnership between DKFZ and University Hospital, Essen, Germany.

Johann Matschke (J)

Institute of Cell Biology (Cancer Research), University Hospital Essen, University of Duisburg-Essen, 45147, Essen, Germany. johann.matschke@uk-essen.de.
German Cancer Consortium (DKTK) partner site Essen a partnership between DKFZ and University Hospital, Essen, Germany. johann.matschke@uk-essen.de.

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