Nuclear factor one B (NFIB) encodes a subtype-specific tumour suppressor in glioblastoma
| Autor: | Kate Goasdoué, Sara Charmsaz, Guy Barry, Fiona M. Smith, Leanne Cooper, Hélène Vidal, Andrew W. Boyd, Michael Piper, Zara C. Bruce, Jens Bunt, Paul R. Jamieson, Brett W. Stringer, Linda J. Richards, Kathleen S. Ensbey, Bryan W. Day |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Pathology medicine.medical_specialty Mice SCID urologic and male genital diseases law.invention Mice 03 medical and health sciences Mice Inbred NOD law glioma Cell Line Tumor Glioma Biomarkers Tumor medicine Animals Humans nuclear factor I B (NFIB) Genes Tumor Suppressor Brain Neoplasms urogenital system business.industry Tumor Suppressor Proteins Mesenchymal stem cell Astrocytoma Cancer tumour suppressor gene medicine.disease female genital diseases and pregnancy complications nervous system diseases 3. Good health NFI Transcription Factors 030104 developmental biology Oncology NFIB Cancer research Heterografts Suppressor glioblastoma (GBM) Ectopic expression Glioblastoma business GBM subtype Research Paper |
| Zdroj: | Oncotarget |
| ISSN: | 1949-2553 |
| DOI: | 10.18632/oncotarget.8720 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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