ArticleComputational and structural biotechnology journal2022
Alterations in 3D chromatin organization contribute to tumorigenesis of
Article in Computational and structural biotechnology journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- PDS5A and TOP2B cooperate for chromatin recruitment via CTCF.bioRxiv : the preprint server for biology · 2026Article
- Endometrial tumorigenesis involves epigenetic plasticity demarcating non-coding somatic mutations and 3D-genome alterations.Genome biology · 2025Article
- Altered chromatin topologies caused by balanced chromosomal translocation lead to central iris hypoplasia.Nature communications · 2024Article
- Pervasive structural heterogeneity rewires glioblastoma chromosomes to sustain patient-specific transcriptional programs.Nature communications · 2024Article
- A potassium-chloride co-transporter with altered genome architecture functions as a suppressor in glioma.Journal of cellular and molecular medicine · 2024Article
- Glioblastoma vaccines: past, present, and opportunities.EBioMedicine · 2024Review
- Expressions of the satellite repeat HSAT5 and transposable elements are implicated in disease progression and survival in glioma.Turkish journal of biology = Turk biyoloji dergisi · 2024Article
- Three-dimensional genome structure and function.MedComm · 2023Review
- Integrating bulk and single-cell RNA sequencing data reveals epithelial-mesenchymal transition molecular subtype and signature to predict prognosis, immunotherapy efficacy, and drug candidates in low-grade gliomas.Frontiers in pharmacology · 2023Article
- Multilevel view on chromatin architecture alterations in cancer.Frontiers in genetics · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Methods: In this study, we explored alterations in 3D chromatin organization of Results: A172 cells showed an elevated chromatin relaxation, and unexpected entanglement of chromosome regions. A genome-wide landscape of switched compartments and differentially expressed genes between HA1800 and A172 cell lines demonstrated that compartment activation reshaped chromatin accessibility and activated tumorigenesis-related genes. Topological associating domain (TAD) analysis revealed that altered TAD domains in A172 also contribute to oncogene activation and tumor repressor deactivation. Interestingly, glioblastoma-derived A172 cells showed a different chromatin loop contact propensity. Genes in tumorigenesis-associated signaling pathways were significantly enriched at the anchor loci of altered chromatin loops. Oncogene activation and tumor repressor deactivation were associated with chromatin loop alteration. Structure variations (SVs) had a dramatic impact on the chromatin conformation of Conclusions: The disordered 3D genomic map and multi-omics data of
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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.