To access the full text documents, please follow this link: http://hdl.handle.net/2445/118923

Title:	GPR56/ADGRG1 inhibits mesenchymal differentiation and radioresistance in glioblastoma
Author:	Moreno Monasterio, Marta; Pedrosa, Leire; Paré Brunet, Laia; Pineda, Estela; Bejarano, Leire; Martínez Soler, Fina; Balasubramaniyan, Veerakumar; Ezhilarasan, Ravesanker; Kallarackal, Naveen; Kim, Sung-Hak; Wang, Jia; Audia, Alessandra; Conroy, Siobhan; Marín Aguilera, Mercedes; Ribalta Farrés, Teresa María; Pujol Farré, Teresa; Herreros, Antoni; Tortosa i Moreno, Avelina; Mira, Helena; Alonso, Marta M.; Gómez-Manzano, Candelaria; Graus Ribas, Francesc; Sulman, Erik P.; Piao, Xianhua; Nakano, Ichiro; Prat Aparicio, Aleix; Bhat, Krishna P.; Iglesia, Núria de la
Notes:	A mesenchymal transition occurs both during the natural evolution of glioblastoma (GBM) and in response to therapy. Here, we report that the adhesion G-protein-coupled receptor, GPR56/ADGRG1, inhibits GBM mesenchymal differentiation and radioresistance. GPR56 is enriched in proneural and classical GBMs and is lost during their transition toward a mesenchymal subtype. GPR56 loss of function promotes mesenchymal differentiation and radioresistance of glioma initiating cells both in vitro and in vivo. Accordingly, a low GPR56-associated signature is prognostic of a poor outcome in GBM patients even within non-G-CIMP GBMs. Mechanistically, we reveal GPR56 as an inhibitor of the nuclear factor kappa B (NF-κB) signaling pathway, thereby providing the rationale by which this receptor prevents mesenchymal differentiation and radioresistance. A pan-cancer analysis suggests that GPR56 might be an inhibitor of the mesenchymal transition across multiple tumor types beyond GBM.
Subject(s):	-Glioma -Tumors -Radioteràpia -Gliomas -Tumors -Radiotherapy
Rights:	cc-by (c) Moreno, Marta et al., 2017 http://creativecommons.org/licenses/by/3.0/es
Document type:	Article Article - Published version
Published by:	Elsevier
Share:

Show full item record