ArticleOncogenesis2022
The SWI/SNF ATPase BRG1 facilitates multiple pro-tumorigenic gene expression programs in SMARCB1-deficient cancer cells.
Article in Oncogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The trial behind it
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
10 citing papers in PubMed, 14 citations in OpenAlex.
- BAF complexes maintain accessibility at stimulus-responsive chromatin and are required for transcriptional stimulus responses.bioRxiv : the preprint server for biology · 2026Article
- Precise modulation of BRG1 levels reveals features of mSWI/SNF dosage sensitivity.Nature genetics · 2025Article
- Pioneering new enhancers by GATA3: role of facilitating transcription factors and chromatin remodeling.Nucleic acids research · 2025Article
- Unraveling the cohesin-chromatin interface: identifying protein interactions that modulate chromosome structure and function.Epigenetics & chromatin · 2025Article
- Loss of SMARCB1 evokes targetable epigenetic vulnerabilities in epithelioid sarcoma.Cancer communications (London, England) · 2025Article
- Opening and changing: mammalian SWI/SNF complexes in organ development and carcinogenesis.Open biology · 2024Review
- Super-Enhancer Dysregulation in Rhabdoid Tumor Cells Is Regulated by the SWI/SNF ATPase BRG1.Cancers · 2024Article
- WRN loss accelerates abnormal adipocyte metabolism in Werner syndrome.Cell & bioscience · 2024Article
- Mutual Regulation of ncRNAs and Chromatin Remodeling Complexes in Normal and Pathological Conditions.International journal of molecular sciences · 2023Review
- Emerging Themes in Mechanisms of Tumorigenesis by SWI/SNF Subunit Mutation.Epigenetics insights · 2022Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Malignant rhabdoid tumor (MRT) is driven by the loss of the SNF5 subunit of the SWI/SNF chromatin remodeling complex and then thought to be maintained by residual SWI/SNF (rSWI/SNF) complexes that remain present in the absence of SNF5. rSWI/SNF subunits colocalize extensively on chromatin with the transcription factor MYC, an oncogene identified as a novel driver of MRT. Currently, the role of rSWI/SNF in modulating MYC activity has neither been delineated nor has a direct link between rSWI/SNF and other oncogenes been uncovered. Here, we expose the connection between rSWI/SNF and oncogenic processes using a well-characterized chemical degrader to deplete the SWI/SNF ATPase, BRG1. Using a combination of gene expression and chromatin accessibility assays we show that rSWI/SNF complexes facilitate MYC target gene expression. We also find that rSWI/SNF maintains open chromatin at sites associated with hallmark cancer genes linked to the AP-1 transcription factor, suggesting that AP-1 may drive oncogenesis in MRT. Interestingly, changes in MYC target gene expression are not overtly connected to the chromatin remodeling function of rSWI/SNF, revealing multiple mechanisms used by rSWI/SNF to control transcription. This work provides an understanding of how residual SWI/SNF complexes may converge on multiple oncogenic processes when normal SWI/SNF function is impaired.
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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.