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

doi:10.18632/oncotarget.8720

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 journal › Article › peer-review

35 Citations (Scopus)

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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 language	English
Pages (from-to)	29306-29320
Number of pages	15
Journal	Oncotarget
Volume	7
Issue number	20
DOIs	https://doi.org/10.18632/oncotarget.8720
Publication status	Published - 17 May 2016
Externally published	Yes

Keywords

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

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.18632/oncotarget.8720Licence: CC BY

Stringer_Nuclear_P2016Final published version, 7.55 MBLicence: CC BY

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Stringer, B. W., Bunt, J., Day, B. W., Barry, G., Jamieson, P. R., Ensbey, K. S., Bruce, Z. C., Goasdoué, K., Vidal, H., Charmsaz, S., Smith, F. M., Cooper, L. T., Piper, M., Boyd, A. W., & Richards, L. J. (2016). Nuclear factor one B (NFIB) encodes a subtype-specific tumour suppressor in glioblastoma. Oncotarget, 7(20), 29306-29320. https://doi.org/10.18632/oncotarget.8720

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

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",

author = "Stringer, {Brett W.} and Jens Bunt and Day, {Bryan W.} and Guy Barry and Jamieson, {Paul R.} and Ensbey, {Kathleen S.} and Bruce, {Zara C.} and Kate Goasdou{\'e} and H{\'e}l{\`e}ne Vidal and Sara Charmsaz and Smith, {Fiona M.} and Cooper, {Leanne T.} and Michael Piper and Boyd, {Andrew W.} and Richards, {Linda J.}",

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doi = "10.18632/oncotarget.8720",

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AU - Stringer, Brett W.

AU - Bunt, Jens

AU - Day, Bryan W.

AU - Barry, Guy

AU - Jamieson, Paul R.

AU - Ensbey, Kathleen S.

AU - Bruce, Zara C.

AU - Goasdoué, Kate

AU - Vidal, Hélène

AU - Charmsaz, Sara

AU - Smith, Fiona M.

AU - Cooper, Leanne T.

AU - Piper, Michael

AU - Boyd, Andrew W.

AU - Richards, Linda J.

PY - 2016/5/17

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AB - 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.

KW - GBM subtype

KW - Glioblastoma (GBM)

KW - Glioma

KW - Nuclear factor I B (NFIB)

KW - Tumour suppressor gene

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ER -

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

Abstract

Keywords

UN SDGs

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