Targeting of Fn14 Prevents Cancer-Induced Cachexia and Prolongs Survival.

Détails

Ressource 1Télécharger: JOhnston2015.pdf (2552.35 [Ko])
Etat: Public
Version: Author's accepted manuscript
ID Serval
serval:BIB_315D44A92CD8
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Targeting of Fn14 Prevents Cancer-Induced Cachexia and Prolongs Survival.
Périodique
Cell
Auteur(s)
Johnston A.J., Murphy K.T., Jenkinson L., Laine D., Emmrich K., Faou P., Weston R., Jayatilleke K.M., Schloegel J., Talbo G., Casey J.L., Levina V., Wong W.W., Dillon H., Sahay T., Hoogenraad J., Anderton H., Hall C., Schneider P., Tanzer M., Foley M., Scott A.M., Gregorevic P., Liu S.Y., Burkly L.C., Lynch G.S., Silke J., Hoogenraad N.J.
ISSN
1097-4172 (Electronic)
ISSN-L
0092-8674
Statut éditorial
Publié
Date de publication
2015
Volume
162
Numéro
6
Pages
1365-1378
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: ppublish
Résumé
The cytokine TWEAK and its cognate receptor Fn14 are members of the TNF/TNFR superfamily and are upregulated in tumors. We found that Fn14, when expressed in tumors, causes cachexia and that antibodies against Fn14 dramatically extended lifespan by inhibiting tumor-induced weight loss although having only moderate inhibitory effects on tumor growth. Anti-Fn14 antibodies prevented tumor-induced inflammation and loss of fat and muscle mass. Fn14 signaling in the tumor, rather than host, is responsible for inducing this cachexia because tumors in Fn14- and TWEAK-deficient hosts developed cachexia that was comparable to that of wild-type mice. These results extend the role of Fn14 in wound repair and muscle development to involvement in the etiology of cachexia and indicate that Fn14 antibodies may be a promising approach to treat cachexia, thereby extending lifespan and improving quality of life for cancer patients.
Pubmed
Web of science
Open Access
Oui
Création de la notice
09/10/2015 7:08
Dernière modification de la notice
20/08/2019 13:16
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