ArticleMolecular cancer research : MCR2014
SNF5/INI1 deficiency redefines chromatin remodeling complex composition during tumor development.
Article in Molecular cancer research : MCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- Panitumumab-Based EGFR Blockade in SMARCB1-Deficient Renal Medullary Carcinoma: Preclinical Basis and Prospective Clinical Activity.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Activating NRF2Cancer gene therapy · 2025Article
- SMARCB1-related schwannomatosis and other SMARCB1-associated phenotypes: clinical spectrum and molecular pathogenesis.Familial cancer · 2025Review
- Chromatin remodeling and cancer: the critical influence of the SWI/SNF complex.Epigenetics & chromatin · 2025Review
- CA-125 as a Biomarker in Renal Medullary Carcinoma: Integrated Molecular Profiling, Functional Characterization, and Prospective Clinical Validation.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Efficacy of glutathione inhibitor eprenetapopt against the vulnerability of glutathione metabolism in SMARCA4-, SMARCB1- and PBRM1-deficient cancer cells.Scientific reports · 2024Article
- BRG1 establishes the neuroectodermal chromatin landscape to restrict dorsal cell fates.Science advances · 2024Article
- Lysine Methylation-Dependent Proteolysis by the Malignant Brain Tumor (MBT) Domain Proteins.International journal of molecular sciences · 2024Review
- Recent insights into the SWI/SNF complex and the molecular mechanism of hSNF5 deficiency in rhabdoid tumors.Cancer medicine · 2023Review
- SMARCB1 regulates the hypoxic stress response in sickle cell trait.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- SMARCB1 Loss in Poorly Differentiated Chordomas Drives Tumor Progression.The American journal of pathology · 2023Article
- The SWI/SNF Complex: A Frequently Mutated Chromatin Remodeling Complex in Cancer.Cancer treatment and research · 2023Article
- The assembly of mammalian SWI/SNF chromatin remodeling complexes is regulated by lysine-methylation dependent proteolysis.Nature communications · 2022Article
- Review
- Article
- Comprehensive Molecular Characterization Identifies Distinct Genomic and Immune Hallmarks of Renal Medullary Carcinoma.Cancer cell · 2020Article
- A heterotrimeric SMARCB1-SMARCC2 subcomplex is required for the assembly and tumor suppression function of the BAF chromatin-remodeling complex.Cell discovery · 2020Article
- Remodeling the cancer epigenome: mutations in the SWI/SNF complex offer new therapeutic opportunities.Expert review of anticancer therapy · 2019Review
- Disruption of mammalian SWI/SNF and polycomb complexes in human sarcomas: mechanisms and therapeutic opportunities.The Journal of pathology · 2018Review
- Dominant-negative SMARCA4 mutants alter the accessibility landscape of tissue-unrestricted enhancers.Nature structural & molecular biology · 2018Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledMalignant rhabdoid tumors (MRT), a pediatric cancer that most frequently appears in the kidney and brain, generally lack SNF5 (SMARCB1/INI1), a subunit of the SWI/SNF chromatin-remodeling complex. Recent studies have established that multiple SWI/SNF complexes exist due to the presence or absence of different complex members. Therefore, the effect of SNF5 loss upon SWI/SNF complex formation was investigated in human MRT cells. MRT cells and primary human tumors exhibited reduced levels of many complex proteins. Furthermore, reexpression of SNF5 increased SWI/SNF complex protein levels without concomitant increases in mRNA. Proteomic analysis, using mass spectrometry, of MRT cells before and after SNF5 reexpression indicated the recruitment of different components into the complex along with the expulsion of others. IP-Western blotting confirmed these results and demonstrated similar changes in other MRT cell lines. Finally, reduced expression of SNF5 in normal human fibroblasts led to altered levels of these same complex members. These data establish that SNF5 loss during MRT development alters the repertoire of available SWI/SNF complexes, generally disrupting those associated with cellular differentiation. These findings support a model where SNF5 inactivation blocks the conversion of growth-promoting SWI/SNF complexes to differentiation-inducing ones. Therefore, restoration of these complexes in tumors cells provides an attractive approach for the treatment of MRTs. IMPLICATIONS: SNF5 loss dramatically alters SWI/SNF complex composition and prevents formation of complexes required for cellular differentiation.
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