ArticleEMBO reports2024
SOX10 mediates glioblastoma cell-state plasticity.
Article in EMBO reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- RNA Expression Signatures in Glioblastoma: A Systematic Review of Tumour Biology and Therapeutic Targets.Oncology research · 2025Pooled it
- Early extracranial dissemination with prolonged survival in IDH-wildtype glioblastoma: case study and comprehensive literature review.CNS oncology · 2026Review
- SOX10 distinguishes oligodendrogliomas from low-grade glioneuronal tumors/low-grade gliomas with oligodendrocyte-like features.The journal of pathology. Clinical research · 2026Article
- [Journal of neuro-oncology · 2026Article
- The expression pattern and prognostic relevance of p120-catenin, COL4A2 and SOX10 in glioma.Frontiers in oncology · 2026Article
- Combinatorial effect of epirubicin and 5-fluorouracil in the treatment of temozolomide-resistant glioblastoma cells.Turkish journal of biology = Turk biyoloji dergisi · 2026Article
- Article
- A new IDH-independent hypermethylation phenotype is associated with astrocyte-like cell state in glioblastoma.Genome biology · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Phenotypic plasticity is a cause of glioblastoma therapy failure. We previously showed that suppressing the oligodendrocyte-lineage regulator SOX10 promotes glioblastoma progression. Here, we analyze SOX10-mediated phenotypic plasticity and exploit it for glioblastoma therapy design. We show that low SOX10 expression is linked to neural stem-cell (NSC)-like glioblastoma cell states and is a consequence of temozolomide treatment in animal and cell line models. Single-cell transcriptome profiling of Sox10-KD tumors indicates that Sox10 suppression is sufficient to induce tumor progression to an aggressive NSC/developmental-like phenotype, including a quiescent NSC-like cell population. The quiescent NSC state is induced by temozolomide and Sox10-KD and reduced by Notch pathway inhibition in cell line models. Combination treatment using Notch and HDAC/PI3K inhibitors extends the survival of mice carrying Sox10-KD tumors, validating our experimental therapy approach. In summary, SOX10 suppression mediates glioblastoma progression through NSC/developmental cell-state transition, including the induction of a targetable quiescent NSC state. This work provides a rationale for the design of tumor therapies based on single-cell phenotypic plasticity analysis.
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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.