ArticleMolecular cell2025
Three-dimensional regulatory hubs support oncogenic programs in glioblastoma.
Article in Molecular cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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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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
7 citing papers in PubMed.
- Global changes in gene expression and splicing in alcoholic liver disease.Scientific reports · 2026Article
- Chromatin architecture and physical constriction cooperate in phenotype switching and cancer cell dissemination.bioRxiv : the preprint server for biology · 2026Article
- KLF5 controls subtype-independent highly interactive enhancers in pancreatic cancer to regulate cell survival.Science advances · 2026Article
- Neuromechanobiology: Bridging Mechanobiology and Neuroscience Through Evidence and Open Questions.Cells · 2026Review
- Integrating biocomputational techniques for vaccine development for glioblastoma multiforme: a possible way of enhancing precision.Frontiers in immunology · 2026Review
- Transcriptional pause release at enhancers mediates cell identity.NAR cancer · 2025Review
- Global Changes in Gene Expression and Splicing in Alcoholic Liver Disease.Research square · 2025Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Dysregulation of enhancer-promoter communication in the three-dimensional (3D) nucleus is increasingly recognized as a potential driver of oncogenic programs. Here, we profiled the 3D enhancer-promoter networks of patient-derived glioblastoma stem cells to identify central regulatory nodes. We focused on hyperconnected 3D hubs and demonstrated that hub-interacting genes exhibit high and coordinated expression at the single-cell level and are associated with oncogenic programs that distinguish glioblastoma from low-grade glioma. Epigenetic silencing of a recurrent hub-with an uncharacterized role in glioblastoma-was sufficient to cause downregulation of hub-connected genes, shifts in transcriptional states, and reduced clonogenicity. Integration of datasets across 16 cancers identified "universal" and cancer-type-specific 3D hubs that enrich for oncogenic programs and factors associated with worse prognosis. Genetic alterations could explain only a small fraction of hub hyperconnectivity and increased activity. Overall, our study provides strong support for the potential central role of 3D regulatory hubs in controlling oncogenic programs and properties.
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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 Socratic graph.