SOCS3 Transactivation by PPARγ Prevents IL-17-Driven Cancer Growth.

Détails

ID Serval
serval:BIB_8768846D2B6D
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
SOCS3 Transactivation by PPARγ Prevents IL-17-Driven Cancer Growth.
Périodique
Cancer Research
Auteur(s)
Berger H., Végran F., Chikh M., Gilardi F., Ladoire S., Bugaut H., Mignot G., Chalmin F., Bruchard M., Derangère V., Chevriaux A., Rébé C., Ryffel B., Pot C., Hichami A., Desvergne B., Ghiringhelli F., Apetoh L.
ISSN
1538-7445 (Electronic)
ISSN-L
0008-5472
Statut éditorial
Publié
Date de publication
2013
Peer-reviewed
Oui
Volume
73
Numéro
12
Pages
3578-3590
Langue
anglais
Résumé
Activation of the transcription factor PPARγ by the n-3 fatty acid docosahexaenoic acid (DHA) is implicated in controlling proinflammatory cytokine secretion, but the intracellular signaling pathways engaged by PPARγ are incompletely characterized. Here, we identify the adapter-encoding gene SOCS3 as a critical transcriptional target of PPARγ. SOCS3 promoter binding and gene transactivation by PPARγ was associated with a repression in differentiation of proinflammatory T-helper (TH)17 cells. Accordingly, TH17 cells induced in vitro displayed increased SOCS3 expression and diminished capacity to produce interleukin (IL)-17 following activation of PPARγ by DHA. Furthermore, naïve CD4 T cells derived from mice fed a DHA-enriched diet displayed less capability to differentiate into TH17 cells. In two different mouse models of cancer, DHA prevented tumor outgrowth and angiogenesis in an IL-17-dependent manner. Altogether, our results uncover a novel molecular pathway by which PPARγ-induced SOCS3 expression prevents IL-17-mediated cancer growth. Cancer Res; 73(12); 3578-90. ©2013 AACR.
Pubmed
Web of science
Open Access
Oui
Création de la notice
18/07/2013 8:30
Dernière modification de la notice
18/02/2020 7:20
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