ArticleOncogene2016
BRG1/SMARCA4 is essential for neuroblastoma cell viability through modulation of cell death and survival pathways.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 2 of them syntheses that pooled it.
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Who cites it
56 citing papers in PubMed, 2 syntheses or guidelines pooled it, 93 citations in OpenAlex.
- Germline variants in SMARCB1 and other members of the BAF chromatin-remodeling complex across human disease entities: a meta-analysis.European journal of human genetics : EJHG · 2018Pooled it
- High expression of SMARCA4 or SMARCA2 is frequently associated with an opposite prognosis in cancer.Scientific reports · 2018Pooled it
- RNA-Seq Profiling Reveals Transcriptional Changes in Phosphorylation-Site Mutants of Brg1.Genes to cells : devoted to molecular & cellular mechanisms · 2026Article
- Epigenetic crosstalk in neuroblastoma development and progression.Frontiers in cell and developmental biology · 2026Review
- The SOX11:SMARCA4 complex is a driver of oncogenic transcriptional programs in mantle cell lymphoma.Blood cancer journal · 2025Article
- Proteomic analysis reveals chromatin remodeling as a potential therapeutical target in neuroblastoma.Journal of translational medicine · 2025Article
- SMARCA4 mutations and expression in lung adenocarcinoma: prognostic significance and impact on the immunotherapy response.FEBS open bio · 2024Article
- Targeting SWI/SNF ATPases reduces neuroblastoma cell plasticity.The EMBO journal · 2024Article
- Mammalian SWI/SNF complex activity regulates POU2F3 and constitutes a targetable dependency in small cell lung cancer.Cancer cell · 2024Article
- Development of an orally bioavailable mSWI/SNF ATPase degrader and acquired mechanisms of resistance in prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Reactivation of the G1 enhancer landscape underlies core circuitry addiction to SWI/SNF.Nucleic acids research · 2024Article
- Germline pathogenicJournal of medical genetics · 2023Article
- Mammalian SWI/SNF chromatin remodeling complexes promote tyrosine kinase inhibitor resistance in EGFR-mutant lung cancer.Cancer cell · 2023Article
- Brg1 controls stemness and metastasis of pancreatic cancer through regulating hypoxia pathway.Oncogene · 2023Article
- SWI/SNF Blockade Disrupts PU.1-Directed Enhancer Programs in Normal Hematopoietic Cells and Acute Myeloid Leukemia.Cancer research · 2023Article
- Therapeutic targeting of CNBP phase separation inhibits ribosome biogenesis and neuroblastoma progression via modulating SWI/SNF complex activity.Clinical and translational medicine · 2023Article
- SOX11 regulates SWI/SNF complex components as member of the adrenergic neuroblastoma core regulatory circuitry.Nature communications · 2023Article
- Delineation of a SMARCA4-specific competing endogenous RNA network and its function in hepatocellular carcinoma.World journal of clinical cases · 2022Article
- Neuroblastoma: When differentiation goes awry.Neuron · 2022Review
- Structural disruption of BAF chromatin remodeller impairs neuroblastoma metastasis by reverting an invasiveness epigenomic program.Molecular cancer · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroblastoma (NB) is a neoplasm of the sympathetic nervous system, and is the most common solid tumor of infancy. NBs are very heterogeneous, with a clinical course ranging from spontaneous regression to resistance to all current forms of treatment. High-risk patients need intense chemotherapy, and only 30-40% will be cured. Relapsed or metastatic tumors acquire multi-drug resistance, raising the need for alternative treatments. Owing to the diverse mechanisms that are responsible of NB chemoresistance, we aimed to target epigenetic factors that control multiple pathways to bypass therapy resistance. We found that the SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily a, member 4 (SMARCA4/BRG1) was consistently upregulated in advanced stages of NB, with high BRG1 levels being indicative of poor outcome. Loss-of-function experiments in vitro and in vivo showed that BRG1 is essential for the proliferation of NB cells. Furthermore, whole-genome transcriptome analysis revealed that BRG1 controls the expression of key elements of oncogenic pathways such as PI3K/AKT and BCL2, which offers a promising new combination therapy for high-risk NB.
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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.