NF1 regulates mesenchymal glioblastoma plasticity and aggressiveness through the AP-1 transcription factor FOSL1

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Abstract: The molecular basis underlying glioblastoma (GBM) heterogeneity and plasticity is not fully understood. Using transcriptomic data of human patient-derived brain tumor stem cell lines (BTSCs), classified based on GBM-intrinsic signatures, we identify the AP-1 transcription factor FOSL1 as a key regulator of the mesenchymal (MES) subtype. We provide a mechanistic basis to the role of the neurofibromatosis type 1 gene (NF1), a negative regulator of the RAS/MAPK pathway, in GBM mesenchymal transformation through the modulation of FOSL1 expression. Depletion of FOSL1 in NF1-mutant human BTSCs and Kras-mutant mouse neural stem cells results in loss of the mesenchymal gene signature and reduction in stem cell properties and in vivo tumorigenic potential. Our data demonstrate that FOSL1 controls GBM plasticity and aggressiveness in response to NF1 alterations

Location: Deutsche Nationalbibliothek Frankfurt am Main

Extent: Online-Ressource

Language: Englisch

Notes: eLife. - 10 (2021) , e64846, ISSN: 2050-084X

Event: Veröffentlichung

(where): Freiburg

(who): Universität

(when): 2021

Creator: Marques, Carolina
Unterkircher, Thomas
Kroon, Paula
Oldrini, Barbara
Izzo, Annalisa
Dramaretska, Yuliia
Ferrarese, Roberto
Kling, Eva
Schnell, Oliver
Nelander, Sven
Wagner, Erwin Friedrich
Bakiri, Latifa
Gargiulo, Gaetano
Carro, Maria Stella
Squatrito, Massimo

DOI: 10.7554/eLife.64846

URN: urn:nbn:de:bsz:25-freidok-2216455

Rights: Kein Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 15.08.2025, 7:39 AM CEST

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Associated

Marques, Carolina
Unterkircher, Thomas
Kroon, Paula
Oldrini, Barbara
Izzo, Annalisa
Dramaretska, Yuliia
Ferrarese, Roberto
Kling, Eva
Schnell, Oliver
Nelander, Sven
Wagner, Erwin Friedrich
Bakiri, Latifa
Gargiulo, Gaetano
Carro, Maria Stella
Squatrito, Massimo
Universität

Time of origin

2021

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NF1 regulates mesenchymal glioblastoma plasticity and aggressiveness through the AP-1 transcription factor FOSL1

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