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Nuclear factor one B (NFIB) encodes a subtype-specific tumour suppressor in glioblastoma

Glioblastoma (GBM) is an essentially incurable and rapidly fatal cancer, with few markers predicting a favourable prognosis. Here we report that the transcription factor NFIB is associated with significantly improved survival in GBM. NFIB expression correlates inversely with astrocytoma grade and is...

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Detalles Bibliográficos
Autores principales: Stringer, Brett W., Bunt, Jens, Day, Bryan W., Barry, Guy, Jamieson, Paul R., Ensbey, Kathleen S., Bruce, Zara C., Goasdoué, Kate, Vidal, Hélène, Charmsaz, Sara, Smith, Fiona M., Cooper, Leanne T., Piper, Michael, Boyd, Andrew W., Richards, Linda J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5045397/
https://www.ncbi.nlm.nih.gov/pubmed/27083054
http://dx.doi.org/10.18632/oncotarget.8720
Descripción
Sumario:Glioblastoma (GBM) is an essentially incurable and rapidly fatal cancer, with few markers predicting a favourable prognosis. Here we report that the transcription factor NFIB is associated with significantly improved survival in GBM. NFIB expression correlates inversely with astrocytoma grade and is lowest in mesenchymal GBM. Ectopic expression of NFIB in low-passage, patient-derived classical and mesenchymal subtype GBM cells inhibits tumourigenesis. Ectopic NFIB expression activated phospho-STAT3 signalling only in classical and mesenchymal GBM cells, suggesting a mechanism through which NFIB may exert its context-dependent tumour suppressor activity. Finally, NFIB expression can be induced in GBM cells by drug treatment with beneficial effects.