IGF1R Axis Inhibition Restores Dendritic Cell Antitumor Response in Ovarian Cancer.
Journal
Translational oncology
ISSN: 1936-5233
Titre abrégé: Transl Oncol
Pays: United States
ID NLM: 101472619
Informations de publication
Date de publication:
Aug 2020
Aug 2020
Historique:
received:
04
02
2020
revised:
14
04
2020
accepted:
16
04
2020
pubmed:
20
5
2020
medline:
20
5
2020
entrez:
20
5
2020
Statut:
ppublish
Résumé
Epithelial ovarian cancer (EOC) is the most lethal gynecological malignancy. The insulin-like growth factor (IGF) system plays a key role in regulating growth and invasiveness in several malignancies, including ovarian cancer. IGF1R targeting showed antiproliferative activity of EOC cells. However, clinical studies failed to show significant benefit. EOC cells suppress antitumor immune responses by inducing dendritic cell (DC) dysfunction. The IGF1 axis can regulate DC maturation. The current study evaluated involvement of the IGF1 axis in DC differentiation in EOC. Studies were conducted on EOC and on a human monocyte cell line. Tissue microarray analysis (TMA) was performed on 36 paraffin blocks from EOC patients. Expression of IGF1R, p53, Ki67, BRCA1, and DC markers was evaluated using immunohistochemistry. Co-culture of EOC cells with DC pretreated with IGF1R inhibitor blocked cancer cell migration. TMA demonstrated higher rate of IGF1R protein expression in patients with advanced (76.9%) as compared to early (40%) EOC. A negative correlation between IGF1R protein expression and the CD1c marker was found. These findings provide evidence that IGF1R axis inhibition could be a therapeutic strategy for ovarian cancer by restoring DC-mediated antitumor immunity.
Identifiants
pubmed: 32428851
pii: S1936-5233(20)30094-2
doi: 10.1016/j.tranon.2020.100790
pmc: PMC7232112
pii:
doi:
Types de publication
Journal Article
Langues
eng
Pagination
100790Informations de copyright
Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Conflicts of Interest The authors declare no conflict of interest.
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