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

Oncotarget. 2016 May 17;7(20):29306-20. doi: 10.18632/oncotarget.8720.

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.

Keywords: GBM subtype; glioblastoma (GBM); glioma; nuclear factor I B (NFIB); tumour suppressor gene.

MeSH terms

  • Animals
  • Biomarkers, Tumor / analysis*
  • Brain Neoplasms / pathology*
  • Cell Line, Tumor
  • Genes, Tumor Suppressor / physiology
  • Glioblastoma / pathology*
  • Heterografts
  • Humans
  • Mice
  • Mice, Inbred NOD
  • Mice, SCID
  • NFI Transcription Factors / metabolism*
  • Tumor Suppressor Proteins / metabolism

Substances

  • Biomarkers, Tumor
  • NFI Transcription Factors
  • NFIB protein, human
  • Tumor Suppressor Proteins