Survival Pathways of HIF-Deficient Tumour Cells: TCA Inhibition, Peroxisomal Fatty Acid Oxidation Activation and an AMPK-PGC-1α Hypoxia Sensor.
1,2-13C2-labelled glucose
AMP-activated kinase
HIF-1β deficiency
Hepa-1 c4 cells
PGC-1α
PPARα
TCA
fatty acid oxidation
hypoxia response
phospho-p38 MAPK
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
14 11 2022
14 11 2022
Historique:
received:
15
10
2022
revised:
09
11
2022
accepted:
09
11
2022
entrez:
26
11
2022
pubmed:
27
11
2022
medline:
30
11
2022
Statut:
epublish
Résumé
The HIF-1 and HIF-2 (HIF1/2) hypoxia responses are frequently upregulated in cancers, and HIF1/2 inhibitors are being developed as anticancer drugs. How could cancers resist anti-HIF1/2 therapy? We studied metabolic and molecular adaptations of HIF-1β-deficient Hepa-1c4, a hepatoma model lacking HIF1/2 signalling, which mimics a cancer treated by a totally effective anti-HIF1/2 agent. [1,2-
Identifiants
pubmed: 36429023
pii: cells11223595
doi: 10.3390/cells11223595
pmc: PMC9688062
pii:
doi:
Substances chimiques
AMP-Activated Protein Kinases
EC 2.7.11.31
Hydrogen Peroxide
BBX060AN9V
Hypoxia-Inducible Factor 1
0
Fatty Acids
0
Adenosine Triphosphate
8L70Q75FXE
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Cancer Research UK
ID : 11359
Pays : United Kingdom
Organisme : Cancer Research UK
ID : C14303/A17197
Pays : United Kingdom
Organisme : Cancer Research UK
ID : C9545/A29580
Pays : United Kingdom
Organisme : Cancer Research UK
ID : C9545/A17197
Pays : United Kingdom
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