ArticleGenes & development2017
Elevated FOXG1 and SOX2 in glioblastoma enforces neural stem cell identity through transcriptional control of cell cycle and epigenetic regulators.
Article in Genes & development, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
82 citing papers in PubMed, 128 citations in OpenAlex.
- Organoids as brain tumour models: bridging the translational gap.Disease models & mechanisms · 2026Review
- Srr2-dependent SOX2 levels govern the chromatin and transcriptional landscape of adult neural stem cell fate decisions in mouse.Genome biology · 2026Article
- Identification of drug candidates against glioblastoma with machine learning and high-throughput screening of heterogeneous cellular models.Digital discovery · 2026Article
- Targeting Autophagy for Otoprotection: Translating Basic Mechanisms into Clinical Strategies.International journal of molecular sciences · 2026Review
- The Role of CRISPR and Its Therapeutic Applications in Glioblastoma.International journal of molecular sciences · 2026Review
- A developmentally regulated long-range enhancer-promoter contact mediates human neural development.bioRxiv : the preprint server for biology · 2026Article
- miR-101/METTL3 axis induces autophagy by interrupting FOXG1/EIF3J-AS1 binding in gliomas.Cell death & disease · 2025Article
- Rapid and Effective Neuronal Conversion of Human Glioblastoma In Vitro and In Vivo Using Potent Small Molecules.Cell proliferation · 2025Article
- Glioblastoma at the crossroads: current understanding and future therapeutic horizons.Signal transduction and targeted therapy · 2025Review
- The lincRNA Pantr1 is a FOXG1 target gene conferring site-specific chromatin binding of FOXG1.Nucleic acids research · 2025Article
- ATRX, OLIG2, MGMT, and IDH2 in Glioblastoma: Essential Molecular Mechanisms and Therapeutic Significance.Medicina (Kaunas, Lithuania) · 2025Article
- Exploring the Dual Roles of Neural Stem Cells in Glioblastoma: Therapeutic Implications and Opportunities.Current stem cell research & therapy · 2025Review
- Single-nucleus RNA sequencing: immature excitatory neurons and transformed glia build human BRAFBrain communications · 2025Article
- Microglia and macrophages in glioblastoma: landscapes and treatment directions.Molecular oncology · 2024Review
- Modelling quiescence exit of neural stem cells reveals a FOXG1-FOXO6 axis.Disease models & mechanisms · 2024Article
- Human stem cell models to unravel brain cancer.BMC cancer · 2024Review
- Functional profiling of murine glioma models highlights targetable immune evasion phenotypes.Acta neuropathologica · 2024Article
- Lineage specification in glioblastoma is regulated by METTL7B.Cell reports · 2024Article
- Deciphering the role of transcription factors in glioblastoma cancer stem cells.Acta biochimica et biophysica Sinica · 2024Review
- Identification of genes with oscillatory expression in glioblastoma: the paradigm of SOX2.Scientific reports · 2024Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
Glioblastoma multiforme (GBM) is an aggressive brain tumor driven by cells with hallmarks of neural stem (NS) cells. GBM stem cells frequently express high levels of the transcription factors FOXG1 and SOX2. Here we show that increased expression of these factors restricts astrocyte differentiation and can trigger dedifferentiation to a proliferative NS cell state. Transcriptional targets include cell cycle and epigenetic regulators (e.g.,
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.