ArticleMolecular cancer2022
Structural disruption of BAF chromatin remodeller impairs neuroblastoma metastasis by reverting an invasiveness epigenomic program.
Article in Molecular cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 13 citations in OpenAlex.
- BAF chromatin remodeling complexes inhibit immediate-early and early, but not late, transcription of herpes simplex virus 1.bioRxiv : the preprint server for biology · 2026Article
- Defining the molecular tolerance-to-damage landscape of SMARCA4 helicase genetic alterations.bioRxiv : the preprint server for biology · 2026Article
- A vitronectin-functionalized ECM-mimetic hydrogel platform for modelling integrin-dependent tumour responses to cilengitide.Materials today. Bio · 2026Article
- Epigenetic Regulation of Trk Receptors and Neurotrophic Signalling in Neuroblastoma: Mechanisms, Plasticity, and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Epigenetic crosstalk in neuroblastoma development and progression.Frontiers in cell and developmental biology · 2026Review
- Interplay Between the Epigenome, the Microenvironment, and the Immune System in Neuroblastoma.Cancers · 2025Review
- Chromatin remodeling and cancer: the critical influence of the SWI/SNF complex.Epigenetics & chromatin · 2025Review
- Cell death pathway regulation by fatty acid metabolism-related genes in neuroblastoma: a multi-omics analysis identifying CHD5 as a novel biomarker.Discover oncology · 2025Article
- Significance of ARID1A in neuroblastoma onset mechanism.Frontiers in oncology · 2025Review
- Targeting SWI/SNF ATPases reduces neuroblastoma cell plasticity.The EMBO journal · 2024Article
- Targeting SWI/SNF Complexes in Cancer: Pharmacological Approaches and Implications.Epigenomes · 2024Review
- Reactivation of the G1 enhancer landscape underlies core circuitry addiction to SWI/SNF.Nucleic acids research · 2024Article
- Unveiling the role of GAS41 in cancer progression.Cancer cell international · 2023Review
- Review
- SOX11 regulates SWI/SNF complex components as member of the adrenergic neuroblastoma core regulatory circuitry.Nature communications · 2023Article
- YY1 transcription factor induces proliferation and aerobic glycolysis of neuroblastoma cells via LDHA regulation.Experimental and therapeutic medicine · 2023Article
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEpigenetic programming during development is essential for determining cell lineages, and alterations in this programming contribute to the initiation of embryonal tumour development. In neuroblastoma, neural crest progenitors block their course of natural differentiation into sympathoadrenergic cells, leading to the development of aggressive and metastatic paediatric cancer. Research of the epigenetic regulators responsible for oncogenic epigenomic networks is crucial for developing new epigenetic-based therapies against these tumours. Mammalian switch/sucrose non-fermenting (mSWI/SNF) ATP-dependent chromatin remodelling complexes act genome-wide translating epigenetic signals into open chromatin states. The present study aimed to understand the contribution of mSWI/SNF to the oncogenic epigenomes of neuroblastoma and its potential as a therapeutic target.
methodsFunctional characterisation of the mSWI/SNF complexes was performed in neuroblastoma cells using proteomic approaches, loss-of-function experiments, transcriptome and chromatin accessibility analyses, and in vitro and in vivo assays.
resultsNeuroblastoma cells contain three main mSWI/SNF subtypes, but only BRG1-associated factor (BAF) complex disruption through silencing of its key structural subunits, ARID1A and ARID1B, impairs cell proliferation by promoting cell cycle blockade. Genome-wide chromatin remodelling and transcriptomic analyses revealed that BAF disruption results in the epigenetic repression of an extensive invasiveness-related expression program involving integrins, cadherins, and key mesenchymal regulators, thereby reducing adhesion to the extracellular matrix and the subsequent invasion in vitro and drastically inhibiting the initiation and growth of neuroblastoma metastasis in vivo.
conclusionsWe report a novel ATPase-independent role for the BAF complex in maintaining an epigenomic program that allows neuroblastoma invasiveness and metastasis, urging for the development of new BAF pharmacological structural disruptors for therapeutic exploitation in metastatic neuroblastoma.
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