The Implications of PDK1-4 on Tumor Energy Metabolism, Aggressiveness and Therapy Resistance.
Warburg effect
aerobic glycolysis
cancer metabolism
oxidative phosphorylation
prostate cancer
pyruvate dehydrogenase kinase
therapy resistance
tricarboxylic acid cycle
Journal
Frontiers in oncology
ISSN: 2234-943X
Titre abrégé: Front Oncol
Pays: Switzerland
ID NLM: 101568867
Informations de publication
Date de publication:
2020
2020
Historique:
received:
14
07
2020
accepted:
13
11
2020
entrez:
1
1
2021
pubmed:
2
1
2021
medline:
2
1
2021
Statut:
epublish
Résumé
A metabolic shift from oxidative phosphorylation (OXPHOS) to glycolysis-known as the Warburg effect-is characteristic for many cancers. It gives the cancer cells a survival advantage in the hypoxic tumor microenvironment and protects them from cytotoxic effects of oxidative damage and apoptosis. The main regulators of this metabolic shift are the pyruvate dehydrogenase complex and pyruvate dehydrogenase kinase (PDK) isoforms 1-4. PDK is known to be overexpressed in several cancers and is associated with bad prognosis and therapy resistance. Whereas the expression of PDK1-3 is tissue specific, PDK4 expression is dependent on the energetic state of the whole organism. In contrast to other PDK isoforms, not only oncogenic, but also tumor suppressive functions of PDK4 have been reported. In tumors that profit from high OXPHOS and high
Identifiants
pubmed: 33384955
doi: 10.3389/fonc.2020.583217
pmc: PMC7771695
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
583217Informations de copyright
Copyright © 2020 Atas, Oberhuber and Kenner.
Déclaration de conflit d'intérêts
LK is a member of the scientific advisory board of CBmed-Center for Biomarker Research in Medicine GmbH. Author MO was employed by COMET centre (K1) CBmed—Center for Biomarker Research in Medicine GmbH. The remaining 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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