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

Onderzoeksoutput: Bijdrage aan tijdschrift › Artikel › peer review

35 Citaten (Scopus)

Samenvatting

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.

Originele taal-2	Engels
Pagina's (van-tot)	29306-29320
Aantal pagina's	15
Tijdschrift	Oncotarget
Volume	7
Nummer van het tijdschrift	20
DOI's	https://doi.org/10.18632/oncotarget.8720
Status	Gepubliceerd - 17 mei 2016
Extern gepubliceerd	Ja

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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",

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year = "2016",

month = may,

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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.

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N2 - 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.

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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U2 - 10.18632/oncotarget.8720

DO - 10.18632/oncotarget.8720

M3 - Article

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SN - 1949-2553

VL - 7

SP - 29306

EP - 29320

JO - Oncotarget

JF - Oncotarget

IS - 20

ER -

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

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