The Ret receptor tyrosine kinase pathway functionally interacts with the ERalpha pathway in breast cancer.

Détails

Ressource 1Demande d'une copie Sous embargo indéterminé.
Etat: Serval
Version: Final published version
ID Serval
serval:BIB_F874E3936774
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
The Ret receptor tyrosine kinase pathway functionally interacts with the ERalpha pathway in breast cancer.
Périodique
Cancer research
Auteur(s)
Boulay A., Breuleux M., Stephan C., Fux C., Brisken C., Fiche M., Wartmann M., Stumm M., Lane H.A., Hynes N.E.
ISSN
1538-7445 (Electronic)
ISSN-L
0008-5472
Statut éditorial
Publié
Date de publication
15/05/2008
Peer-reviewed
Oui
Volume
68
Numéro
10
Pages
3743-3751
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
A limited number of receptor tyrosine kinases (e.g., ErbB and fibroblast growth factor receptor families) have been genetically linked to breast cancer development. Here, we investigated the contribution of the Ret receptor tyrosine kinase to breast tumor biology. Ret was expressed in primary breast tumors and cell lines. In estrogen receptor (ER)alpha-positive MCF7 and T47D lines, the ligand (glial-derived neurotrophic factor) activated signaling pathways and increased anchorage-independent proliferation in a Ret-dependent manner, showing that Ret signaling is functional in breast tumor cells. Ret expression was induced by estrogens and Ret signaling enhanced estrogen-driven proliferation, highlighting the functional interaction of Ret and ER pathways. Furthermore, Ret was detected in primary cancers, and there were higher Ret levels in ERalpha-positive tumors. In summary, we showed that Ret is a novel proliferative pathway interacting with ER signaling in vitro. Expression of Ret in primary breast tumors suggests that Ret might be a novel therapeutic target in breast cancer.

Mots-clé
Agar/chemistry, Biopsy, Breast Neoplasms/metabolism, Cell Line, Tumor, Cell Proliferation, Estrogen Receptor alpha/metabolism, Fibroblasts/metabolism, Gene Expression Regulation, Neoplastic, Glial Cell Line-Derived Neurotrophic Factor/metabolism, Humans, Models, Biological, Protein Binding, Proto-Oncogene Proteins c-ret/metabolism, Signal Transduction, Steroids/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
06/06/2008 11:28
Dernière modification de la notice
09/05/2019 3:41
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