ArticleOncotarget2014
The silencing of the SWI/SNF subunit and anticancer gene BRM in Rhabdoid tumors.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- BRM Promoter Polymorphisms and Survival of Advanced Non-Small Cell Lung Cancer Patients in the Princess Margaret Cohort and CCTG BR.24 Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Trial
- Delineating SWI/SNF gene and subtype expression in cancer.Epigenetics & chromatin · 2026Article
- Children's Oncology Group's 2023 blueprint for research: Renal tumors.Pediatric blood & cancer · 2023Article
- (mis)-Targeting of SWI/SNF complex(es) in cancer.Cancer metastasis reviews · 2023Review
- SMARCB1 Loss in Poorly Differentiated Chordomas Drives Tumor Progression.The American journal of pathology · 2023Article
- Whole-genome characterization of myoepithelial carcinomas of the soft tissue.Cold Spring Harbor molecular case studies · 2022Article
- Quis Custodiet Ipsos Custodes (Who Controls the Controllers)? Two Decades of Studies on HDAC9.Life (Basel, Switzerland) · 2021Review
- The SWI/SNF complex in cancer - biology, biomarkers and therapy.Nature reviews. Clinical oncology · 2020Review
- Article
- High HDAC9 is associated with poor prognosis and promotes malignant progression in pancreatic ductal adenocarcinoma.Molecular medicine reports · 2020Article
- BRM: the core ATPase subunit of SWI/SNF chromatin-remodelling complex-a tumour suppressor or tumour-promoting factor?Epigenetics & chromatin · 2019Review
- Ponatinib Shows Potent Antitumor Activity in Small Cell Carcinoma of the Ovary Hypercalcemic Type (SCCOHT) through Multikinase Inhibition.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Article
- PRC2-mediated repression of SMARCA2 predicts EZH2 inhibitor activity in SWI/SNF mutant tumors.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Clinicopathological and molecular characterization of SMARCA4-deficient thoracic sarcomas with comparison to potentially related entities.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2017Article
- Article
- The disparate origins of ovarian cancers: pathogenesis and prevention strategies.Nature reviews. Cancer · 2017Review
- Mechanism of BRG1 silencing in primary cancers.Oncotarget · 2016Article
- Review
- Epigenetically maintained SW13+ and SW13- subtypes have different oncogenic potential and convert with HDAC1 inhibition.BMC cancer · 2016Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rhabdoid sarcomas are highly malignant tumors that usually occur in young children. A key to the genesis of this tumor is the mutational loss of the BAF47 gene as well as the widespread epigenetic suppression of other key anticancer genes. The BRM gene is one such epigenetically silenced gene in Rhabdoid tumors. This gene codes for an ATPase catalytic subunit that shifts histones and opens the chromatin. We show that BRM is an epigenetically silenced gene in 10/11 Rhabdoid cell lines and in 70% of Rhabdoid tumors. Moreover, BRM can be induced by BAF47 re-expression and by Flavopiridol. By selective shRNAi knockdown of BRM, we show that BRM re-expression is necessary for growth inhibition by BAF47 re-expression or Flavopiridol application. Similar to lung cancer cell lines, we found that HDAC3, HDAC9, MEF2D and GATA3 controlled BRM silencing and that HDAC9 was overexpressed in Rhabdoid cancer cell lines. In primary BRM-deficient Rhabdoid tumors, HDAC9 was also found to be highly overexpressed. Two insertional BRM promoter polymorphisms contribute to BRM silencing, but only the -1321 polymorphism correlated with BRM silencing in Rhabdoid cell lines. To determine how these polymorphisms were tied to BRM silencing, we conducted ChIP assays and found that both HDAC9 and MEF2D bound to the BRM promoter at or near these polymorphic sites. Using BRM promoter swap experiments, we indirectly showed that both HDAC9 and MEF2D bound to these polymorphic sites. Together, these data show that the mechanism of BRM silencing contributes to the pathogenesis of Rhabdoid tumors and appears to be conserved among tumor types.
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