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

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 regul...

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Vydáno v:eLife Ročník 10
Hlavní autoři: Marques, Carolina, Unterkircher, Thomas, Kroon, Paula, Oldrini, Barbara, Izzo, Annalisa, Dramaretska, Yuliia, Ferrarese, Roberto, Kling, Eva, Schnell, Oliver, Nelander, Sven, Wagner, Erwin F, Bakiri, Latifa, Gargiulo, Gaetano, Carro, Maria Stella, Squatrito, Massimo
Médium: Journal Article
Jazyk:angličtina
Vydáno: England eLife Sciences Publications Ltd 17.08.2021
eLife Sciences Publications, Ltd
Témata:
Activator protein 1
Brain cancer
Brain Neoplasms - genetics
Brain stem
Brain tumors
Cancer Biology
Cell cycle
Cell Line, Tumor
Classification
Datasets
FOSL1
FRA-1
GBM
Gene expression
Gene Expression Regulation, Neoplastic
Glioblastoma
Glioblastoma - genetics
Humans
MAP kinase
mesenchymal
Mesenchyme
Mutants
Mutation
Neoplastic Stem Cells - pathology
Neural stem cells
Neurofibromatosis
Neurofibromin 1
Neurofibromin 1 - genetics
Neurofibromin 1 - metabolism
NF1
Proto-Oncogene Proteins c-fos - genetics
Proto-Oncogene Proteins c-fos - metabolism
Stem cell transplantation
Stem cells
Transcription factors
Transcriptomics
Tumor cell lines
Tumors
FOSL1
mouse
GBM
mesenchymal
NF1
FRA-1
cancer biology
human
ISSN:2050-084X, 2050-084X
On-line přístup:Získat plný text
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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.
AbstractList 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.
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.
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.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.
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 as a key regulator of the mesenchymal (MES) subtype. We provide a mechanistic basis to the role of the neurofibromatosis type 1 gene ( ), a negative regulator of the RAS/MAPK pathway, in GBM mesenchymal transformation through the modulation of expression. Depletion of in -mutant human BTSCs and -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 controls GBM plasticity and aggressiveness in response to alterations.
Author Schnell, Oliver
Izzo, Annalisa
Gargiulo, Gaetano
Carro, Maria Stella
Nelander, Sven
Unterkircher, Thomas
Wagner, Erwin F
Kling, Eva
Bakiri, Latifa
Marques, Carolina
Kroon, Paula
Ferrarese, Roberto
Dramaretska, Yuliia
Oldrini, Barbara
Squatrito, Massimo
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  organization: Department of Neurosurgery, Faculty of Medicine Freiburg, Freiburg, Germany
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  organization: Seve Ballesteros Foundation Brain Tumor Group, Spanish National Cancer Research Centre, Madrid, Spain
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  organization: Department of Neurosurgery, Faculty of Medicine Freiburg, Freiburg, Germany
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  surname: Nelander
  fullname: Nelander, Sven
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  organization: Genes, Development, and Disease Group, Spanish National Cancer Research Centre, Madrid, Spain, Laboratory Medicine Department, Medical University of Vienna, Vienna, Austria, Dermatology Department, Medical University of Vienna, Vienna, Austria
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/34399888$$D View this record in MEDLINE/PubMed
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Copyright 2021, Marques et al.
2021, Marques et al. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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Keywords FOSL1
mouse
GBM
mesenchymal
NF1
FRA-1
cancer biology
human
Language English
License 2021, Marques et al.
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Snippet The molecular basis underlying glioblastoma (GBM) heterogeneity and plasticity is not fully understood. Using transcriptomic data of human patient-derived...
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SubjectTerms Activator protein 1
Brain cancer
Brain Neoplasms - genetics
Brain stem
Brain tumors
Cancer Biology
Cell cycle
Cell Line, Tumor
Classification
Datasets
FOSL1
FRA-1
GBM
Gene expression
Gene Expression Regulation, Neoplastic
Glioblastoma
Glioblastoma - genetics
Humans
MAP kinase
mesenchymal
Mesenchyme
Mutants
Mutation
Neoplastic Stem Cells - pathology
Neural stem cells
Neurofibromatosis
Neurofibromin 1
Neurofibromin 1 - genetics
Neurofibromin 1 - metabolism
NF1
Proto-Oncogene Proteins c-fos - genetics
Proto-Oncogene Proteins c-fos - metabolism
Stem cell transplantation
Stem cells
Transcription factors
Transcriptomics
Tumor cell lines
Tumors
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Title NF1 regulates mesenchymal glioblastoma plasticity and aggressiveness through the AP-1 transcription factor FOSL1
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