The potential for citrate to reinforce epigenetic therapy by promoting apoptosis.


Journal

Trends in endocrinology and metabolism: TEM
ISSN: 1879-3061
Titre abrégé: Trends Endocrinol Metab
Pays: United States
ID NLM: 9001516

Informations de publication

Date de publication:
10 2023
Historique:
received: 15 03 2023
revised: 04 07 2023
accepted: 18 07 2023
medline: 15 9 2023
pubmed: 8 8 2023
entrez: 7 8 2023
Statut: ppublish

Résumé

Epigenetic drugs induce ATP depletion, promoting a glycolysis-to-oxidative phosphorylation (OXPHOS) shift which sometimes favors tumor growth by promoting necroptosis over apoptosis. To restore effective apoptosis in tumors, we propose that the administration of citrate could inhibit ATP production, activate caspase-8 (a key necroptosis inhibitor), and downregulate key anti-apoptotic proteins (Bcl-xL and MCL1).

Identifiants

pubmed: 37550099
pii: S1043-2760(23)00133-9
doi: 10.1016/j.tem.2023.07.002
pii:
doi:

Substances chimiques

Citric Acid 2968PHW8QP
bcl-X Protein 0
Citrates 0
Adenosine Triphosphate 8L70Q75FXE

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

586-589

Informations de copyright

Copyright © 2023 Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The authors have no conflicts of interest to declare.

Auteurs

Philippe Icard (P)

Normandie University, UNICAEN, INSERM U1086 Interdisciplinary Research Unit for Cancer Prevention and Treatment, Caen, France; Service de Chirurgie Thoracique, Hôpital Cochin, Hôpitaux Universitaires Paris Centre, APHP, Université Paris-Descartes, Paris, France. Electronic address: philippe.icard@aphp.fr.

Marco Alifano (M)

Service de Chirurgie Thoracique, Hôpital Cochin, Hôpitaux Universitaires Paris Centre, APHP, Université Paris-Descartes, Paris, France; INSERM U1138, Integrative Cancer Immunology, University of Paris, 75006 Paris, France.

Luca Simula (L)

Cochin Institute, INSERM U1016, CNRS UMR8104, University of Paris-Cité, Paris, 75014, France.

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Classifications MeSH