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dc.contributor.author | Moreno Monasterio, Marta |
---|---|
dc.contributor.author | Pedrosa, Leire |
dc.contributor.author | Paré Brunet, Laia |
dc.contributor.author | Pineda, Estela |
dc.contributor.author | Bejarano, Leire |
dc.contributor.author | Martínez Soler, Fina |
dc.contributor.author | Balasubramaniyan, Veerakumar |
dc.contributor.author | Ezhilarasan, Ravesanker |
dc.contributor.author | Kallarackal, Naveen |
dc.contributor.author | Kim, Sung-Hak |
dc.contributor.author | Wang, Jia |
dc.contributor.author | Audia, Alessandra |
dc.contributor.author | Conroy, Siobhan |
dc.contributor.author | Marín Aguilera, Mercedes |
dc.contributor.author | Ribalta Farrés, Teresa María |
dc.contributor.author | Pujol Farré, Teresa |
dc.contributor.author | Herreros, Antoni |
dc.contributor.author | Tortosa i Moreno, Avelina |
dc.contributor.author | Mira, Helena |
dc.contributor.author | Alonso, Marta M. |
dc.contributor.author | Gómez-Manzano, Candelaria |
dc.contributor.author | Graus Ribas, Francesc |
dc.contributor.author | Sulman, Erik P. |
dc.contributor.author | Piao, Xianhua |
dc.contributor.author | Nakano, Ichiro |
dc.contributor.author | Prat Aparicio, Aleix |
dc.contributor.author | Bhat, Krishna P. |
dc.contributor.author | Iglesia, Núria de la |
dc.date | 2018-01-09T12:16:53Z |
dc.date | 2018-01-09T12:16:53Z |
dc.date | 2017-11-21 |
dc.date | 2018-01-09T12:16:54Z |
dc.identifier | 2211-1247 |
dc.identifier | 674462 |
dc.identifier | 29166609 |
dc.identifier.uri | http://hdl.handle.net/2445/118923 |
dc.description | 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. |
dc.format | 15 p. |
dc.format | application/pdf |
dc.language | eng |
dc.publisher | Elsevier |
dc.relation | Reproducció del document publicat a: https://doi.org/10.1016/j.celrep.2017.10.083 |
dc.relation | Cell Reports, 2017, vol. 21, num. 8, p. 2183-2197 |
dc.relation | https://doi.org/10.1016/j.celrep.2017.10.083 |
dc.rights | cc-by (c) Moreno, Marta et al., 2017 |
dc.rights | http://creativecommons.org/licenses/by/3.0/es |
dc.rights | info:eu-repo/semantics/openAccess |
dc.subject | Glioma |
dc.subject | Tumors |
dc.subject | Radioteràpia |
dc.subject | Gliomas |
dc.subject | Tumors |
dc.subject | Radiotherapy |
dc.title | GPR56/ADGRG1 inhibits mesenchymal differentiation and radioresistance in glioblastoma |
dc.type | info:eu-repo/semantics/article |
dc.type | info:eu-repo/semantics/publishedVersion |