Insulin Receptor Isoform A Modulates Metabolic Reprogramming of Breast Cancer Cells in Response to IGF2 and Insulin Stimulation.
Antimetabolites
/ pharmacology
Breast Neoplasms
/ metabolism
Cell Movement
/ drug effects
Cell Proliferation
/ drug effects
Deoxyglucose
/ pharmacology
Female
Glycolysis
Humans
Insulin
/ metabolism
Insulin-Like Growth Factor II
/ metabolism
MCF-7 Cells
Metformin
/ pharmacology
Mitochondria
/ drug effects
Protein Isoforms
/ genetics
Receptor, IGF Type 1
/ genetics
IGF1R
IGF2
aerobic glycolysis
breast cancer
insulin receptor isoform A
metabolic flexibility
metabolic reprogramming
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
01 09 2019
01 09 2019
Historique:
received:
05
08
2019
revised:
27
08
2019
accepted:
29
08
2019
entrez:
5
9
2019
pubmed:
5
9
2019
medline:
15
5
2020
Statut:
epublish
Résumé
Previously published work has demonstrated that overexpression of the insulin receptor isoform A (IR-A) might play a role in cancer progression and metastasis. The IR has a predominant metabolic role in physiology, but the potential role of IR-A in cancer metabolic reprogramming is unknown. We aimed to characterize the metabolic impact of IR-A and its ligand insulin like growth factor 2 (IGF2) in human breast cancer (BC) cells. To establish autocrine IGF2 action, we generated human BC cells MCF7 overexpressing the human IGF2, while we focused on the metabolic effect of IR-A by stably infecting
Identifiants
pubmed: 31480557
pii: cells8091017
doi: 10.3390/cells8091017
pmc: PMC6770491
pii:
doi:
Substances chimiques
Antimetabolites
0
IGF1R protein, human
0
IGF2 protein, human
0
Insulin
0
Protein Isoforms
0
Insulin-Like Growth Factor II
67763-97-7
Metformin
9100L32L2N
Deoxyglucose
9G2MP84A8W
Receptor, IGF Type 1
EC 2.7.10.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
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