Nuclear factor one B (NFIB) encodes a subtype-specific tumour suppressor in glioblastoma
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Brett W. Stringer1,2, Jens Bunt3, Bryan W. Day1,2, Guy Barry3, Paul R. Jamieson1,2, Kathleen S. Ensbey1,2, Zara C. Bruce1,2, Kate Goasdoué1,2, Hélène Vidal1,2, Sara Charmsaz2, Fiona M. Smith2, Leanne T. Cooper2, Michael Piper3,4, Andrew W. Boyd1,2,5,*, Linda J. Richards3,4,*
1Brain Cancer Research Unit, QIMR Berghofer Medical Research Institute, Brisbane, 4006, Queensland, Australia
2Leukaemia Foundation Research Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, 4006, Queensland, Australia
3Queensland Brain Institute, The University of Queensland, Brisbane, 4072, Queensland, Australia
4School of Biomedical Sciences, The University of Queensland, Brisbane, 4072, Queensland, Australia
5Department of Medicine, The University of Queensland, Brisbane, 4072, Queensland, Australia
Brett W. Stringer, e-mail: [email protected]
Michael Piper, e-mail: [email protected]
Andrew W. Boyd, e-mail: [email protected]
Linda J. Richards, e-mail: [email protected]
Keywords: glioblastoma (GBM), glioma, nuclear factor I B (NFIB), tumour suppressor gene, GBM subtype
Received: November 30, 2015 Accepted: March 28, 2016 Published: April 13, 2016
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.
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