ArticleGenome biology2025
A new IDH-independent hypermethylation phenotype is associated with astrocyte-like cell state in glioblastoma.
Article in Genome biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- EDNRB-dependent endothelin signaling reduces proliferation and promotes proneural-to-mesenchymal transition in gliomas.Molecular oncology · 2026Article
- Astrocytes in neuroinflammation and brain cancer.Molecular biomedicine · 2026Review
- The Natural Triterpenoid Alisol B Overcomes Temozolomide Resistance in Glioblastoma Through Multi-Target Mechanisms: Coordinated Epigenetic, Metabolic, and Cell-Cycle Reprogramming.International journal of molecular sciences · 2026Article
- TUBB2A and TM4SF1 Methylation Define Prognostic Subgroups in Adult-Type Diffuse Glioma.Cancers · 2026Article
- Targeting TRIM25 as a therapeutic strategy to enhance ferroptosis in glioblastoma cells.Journal of nanobiotechnology · 2026Article
- Intermediately Methylated Regions in Normal Cells Are Epimutation Hotspots in Cancer.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
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Abstract
backgroundDNA methylation plays a crucial role in cancer development and progression and has been linked to genetically and clinically distinct tumor classes, including IDH-mutated and IDH-wildtype adult-type diffuse gliomas. Here, we identify a CpG-island methylator phenotype (CIMP) that characterizes the receptor tyrosine kinase 2 (RTK2) subtype of IDH-wildtype glioblastoma.
resultsThis RTK2-CIMP affects genomic locations and cell functions distinct from those of IDH mutation-associated IDH-CIMP and suppresses the expression of its target genes. The RTK2-CIMP-region chromatin is characterized by a combination of repressive and activating marks, including polycomb-associated H3K27me3 and enhancer-associated H3K4me1, consistent with DNA methylation-mediated silencing of genes with bivalent-state promoters in neural progenitor cells. Functionally, RTK2-CIMP affects neuronal lineage genes and is significantly associated with astrocyte-like glioblastoma, suggesting that RTK2-CIMP is an epigenetic signature of the astrocyte-like cell state. Furthermore, we demonstrate that RTK2-CIMP can be induced by genetic manipulation in glioblastoma cells.
conclusionsOur results suggest that RTK2-CIMP is a key contributor to cell-state plasticity in glioblastoma.
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