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

نویسندگان

  • 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
چکیده

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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عنوان ژورنال:

دوره 7  شماره 

صفحات  -

تاریخ انتشار 2016