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

Brett W. Stringer, Jens Bunt, Bryan W. Day, Guy Barry, Paul R. Jamieson, Kathleen S. Ensbey, Zara C. Bruce, Kate Goasdoué, Hélène Vidal, Sara Charmsaz, Fiona M. Smith, Leanne T. Cooper, Michael Piper, Andrew W. Boyd, Linda J. Richards

Research output: Contribution to journalArticlepeer-review

20 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)29306-29320
Number of pages15
JournalOncotarget
Volume7
Issue number20
DOIs
Publication statusPublished - 17 May 2016
Externally publishedYes

Keywords

  • GBM subtype
  • Glioblastoma (GBM)
  • Glioma
  • Nuclear factor I B (NFIB)
  • Tumour suppressor gene

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