Metabolic stress induces GD2
Animals
Blood Glucose
/ analysis
Cell Line, Tumor
Female
Ferroptosis
/ drug effects
Gangliosides
/ metabolism
Glutamine
/ metabolism
Humans
Metabolomics
/ methods
Mice
Neoplastic Stem Cells
/ drug effects
Phenotype
Small Molecule Libraries
/ administration & dosage
Triple Negative Breast Neoplasms
/ drug therapy
Xenograft Model Antitumor Assays
Journal
British journal of cancer
ISSN: 1532-1827
Titre abrégé: Br J Cancer
Pays: England
ID NLM: 0370635
Informations de publication
Date de publication:
03 2022
03 2022
Historique:
received:
14
04
2021
accepted:
09
11
2021
revised:
25
10
2021
pubmed:
24
11
2021
medline:
11
3
2022
entrez:
23
11
2021
Statut:
ppublish
Résumé
Metabolic stress resulting from nutrient deficiency is one of the hallmarks of a growing tumour. Here, we tested the hypothesis that metabolic stress induces breast cancer stem-like cell (BCSC) phenotype in triple-negative breast cancer (TNBC). Flow cytometry for GD2 expression, mass spectrometry and Ingenuity Pathway Analysis for metabolomics, bioinformatics, in vitro tumorigenesis and in vivo models were used. Serum/glucose deprivation not only increased stress markers but also enhanced GD2 Here, we show metabolic stress results in GD2
Sections du résumé
BACKGROUND
Metabolic stress resulting from nutrient deficiency is one of the hallmarks of a growing tumour. Here, we tested the hypothesis that metabolic stress induces breast cancer stem-like cell (BCSC) phenotype in triple-negative breast cancer (TNBC).
METHODS
Flow cytometry for GD2 expression, mass spectrometry and Ingenuity Pathway Analysis for metabolomics, bioinformatics, in vitro tumorigenesis and in vivo models were used.
RESULTS
Serum/glucose deprivation not only increased stress markers but also enhanced GD2
CONCLUSION
Here, we show metabolic stress results in GD2
Identifiants
pubmed: 34811508
doi: 10.1038/s41416-021-01636-y
pii: 10.1038/s41416-021-01636-y
pmc: PMC8854435
doi:
Substances chimiques
Blood Glucose
0
Gangliosides
0
Small Molecule Libraries
0
Glutamine
0RH81L854J
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
615-627Subventions
Organisme : NCI NIH HHS
ID : R01 CA220297
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA125123
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA216426
Pays : United States
Informations de copyright
© 2021. The Author(s), under exclusive licence to Springer Nature Limited.
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