ArticleJournal of cellular physiology2015
The SWI/SNF ATPases Are Required for Triple Negative Breast Cancer Cell Proliferation.
Article in Journal of cellular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 43 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- High expression of SMARCA4 or SMARCA2 is frequently associated with an opposite prognosis in cancer.Scientific reports · 2018Pooled it
- Effect of mAnimals : an open access journal from MDPI · 2025Article
- Chromatin remodeling complexes: architects influencing breast cancer progression.Frontiers in cell and developmental biology · 2025Review
- Research progress of SWI/SNF complex in breast cancer.Epigenetics & chromatin · 2024Review
- The role of chromatin remodeler SMARCA4/BRG1 in brain cancers: a potential therapeutic target.Oncogene · 2023Review
- Brg1 controls stemness and metastasis of pancreatic cancer through regulating hypoxia pathway.Oncogene · 2023Article
- A Swedish Familial Genome-Wide Haplotype Analysis Identified Five Novel Breast Cancer Susceptibility Loci on 9p24.3, 11q22.3, 15q11.2, 16q24.1 and Xq21.31.International journal of molecular sciences · 2023Article
- Epigenome Programming by H3.3K27M Mutation Creates a Dependence of Pediatric Glioma on SMARCA4.Cancer discovery · 2022Article
- Mechanisms behind context-dependent role of glucocorticoids in breast cancer progression.Cancer metastasis reviews · 2022Review
- Microarray data reveal potential genes that regulate triple-negative breast cancer.The Journal of international medical research · 2022Article
- SNF5 promotes cell proliferation and immune evasion in non-small cell lung cancer.Bioengineered · 2022Article
- SWI/SNF Chromatin Remodeling Enzymes in Melanoma.Epigenomes · 2022Review
- Identification of key genes involved in tamoxifen-resistant breast cancer using bioinformatics analysis.Translational cancer research · 2021Article
- Comprehensive characterization of distinct genetic alterations in metastatic breast cancer across various metastatic sites.NPJ breast cancer · 2021Article
- SOX4 and SMARCA4 cooperatively regulate PI3k signaling through transcriptional activation of TGFBR2.NPJ breast cancer · 2021Article
- The SWI/SNF subunit SMARCD3 regulates cell cycle progression and predicts survival outcome in ER+ breast cancer.Breast cancer research and treatment · 2021Article
- Identification and Validation of SNP-Containing Genes With Prognostic Value in Gastric CancerFrontiers in oncology · 2021Article
- SWI/SNF chromatin remodeling complex and glucose metabolism are deregulated in advanced bladder cancer.IUBMB life · 2020Article
- BRG1 Activates Proliferation and Transcription of Cell Cycle-Dependent Genes in Breast Cancer Cells.Cancers · 2020Article
- Interaction Proteomics Identifies ERbeta Association with Chromatin Repressive Complexes to Inhibit Cholesterol Biosynthesis and Exert An Oncosuppressive Role in Triple-negative Breast Cancer.Molecular & cellular proteomics : MCP · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
19 authors at 8 institutions in 1 country.
Funding
Abstract
The Brahma (BRM) and Brahma-related Gene 1 (BRG1) ATPases are highly conserved homologs that catalyze the chromatin remodeling functions of the multi-subunit human SWI/SNF chromatin remodeling enzymes in a mutually exclusive manner. SWI/SNF enzyme subunits are mutated or missing in many cancer types, but are overexpressed without apparent mutation in other cancers. Here, we report that both BRG1 and BRM are overexpressed in most primary breast cancers independent of the tumor's receptor status. Knockdown of either ATPase in a triple negative breast cancer cell line reduced tumor formation in vivo and cell proliferation in vitro. Fewer cells in S phase and an extended cell cycle progression time were observed without any indication of apoptosis, senescence, or alterations in migration or attachment properties. Combined knockdown of BRM and BRG1 showed additive effects in the reduction of cell proliferation and time required for completion of cell cycle, suggesting that these enzymes promote cell cycle progression through independent mechanisms. Knockout of BRG1 or BRM using CRISPR/Cas9 technology resulted in the loss of viability, consistent with a requirement for both enzymes in triple negative breast cancer cells.
Indexed as
Identifiers
What OpenQuestion holds
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.