ArticleOncotarget2015
SWI/SNF complexes are required for full activation of the DNA-damage response.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Primary Renal Synovial Sarcoma and Clinical and Pathological Findings: a Systematic Review.Current urology reports · 2021Pooled it
- Stage IV SMARCA4-Deficient Undifferentiated Malignant Neoplasm With Primary Cutaneous Origin and Early Distant Metastases.Case reports in dermatological medicine · 2026Article
- Determination of Differential miRNA Expression Profile in People with Noise-Induced Hearing Loss.International journal of molecular sciences · 2025Article
- Article
- Mutual Regulation of ncRNAs and Chromatin Remodeling Complexes in Normal and Pathological Conditions.International journal of molecular sciences · 2023Review
- CLOCK and TIMELESS regulate rhythmic occupancy of the BRAHMA chromatin-remodeling protein at clock gene promoters.PLoS genetics · 2023Article
- SMARCA4/2 loss inhibits chemotherapy-induced apoptosis by restricting IP3R3-mediated CaNature communications · 2021Article
- Zinc finger protein E4F1 cooperates with PARP-1 and BRG1 to promote DNA double-strand break repair.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The SWI/SNF ATPase BRG1 stimulates DNA end resection and homologous recombination by reducing nucleosome density at DNA double strand breaks and by promoting the recruitment of the CtIP nuclease.Cell cycle (Georgetown, Tex.) · 2020Article
- An Azidoribose Probe to Track Ketoamine Adducts in Histone Ribose Glycation.Journal of the American Chemical Society · 2020Article
- Article
- Combining epigenetic drugs with other therapies for solid tumours - past lessons and future promise.Nature reviews. Clinical oncology · 2020Review
- The Role of RNA Splicing Factors in Cancer: Regulation of Viral and Human Gene Expression in Human Papillomavirus-Related Cervical Cancer.Frontiers in cell and developmental biology · 2020Review
- Chromatin Remodeling Factor BRG1 Regulates Stemness and Chemosensitivity of Glioma Initiating Cells.Stem cells (Dayton, Ohio) · 2018Article
- Article
- ATR Is a Therapeutic Target in Synovial Sarcoma.Cancer research · 2017Article
- Modulation of the Fanconi anemia pathwayOncotarget · 2017Article
- Quantification of cell cycle kinetics by EdU (5-ethynyl-2'-deoxyuridine)-coupled-fluorescence-intensity analysis.Oncotarget · 2017Article
- The SWI/SNF ATP-dependent nucleosome remodeler promotes resection initiation at a DNA double-strand break in yeast.Nucleic acids research · 2017Article
- The BRG1 ATPase of human SWI/SNF chromatin remodeling enzymes as a driver of cancer.Epigenomics · 2017Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
SWI/SNF complexes utilize BRG1 (also known as SMARCA4) or BRM (also known as SMARCA2) as alternative catalytic subunits with ATPase activity to remodel chromatin. These chromatin-remodeling complexes are required for mammalian development and are mutated in ~20% of all human primary tumors. Yet our knowledge of their tumor-suppressor mechanism is limited. To investigate the role of SWI/SNF complexes in the DNA-damage response (DDR), we used shRNAs to deplete BRG1 and BRM and then exposed these cells to a panel of 6 genotoxic agents. Compared to controls, the shRNA knockdown cells were hypersensitive to certain genotoxic agents that cause double-strand breaks (DSBs) associated with stalled/collapsed replication forks but not to ionizing radiation-induced DSBs that arise independently of DNA replication. These findings were supported by our analysis of DDR kinases, which demonstrated a more prominent role for SWI/SNF in the activation of the ATR-Chk1 pathway than the ATM-Chk2 pathway. Surprisingly, γH2AX induction was attenuated in shRNA knockdown cells exposed to a topoisomerase II inhibitor (etoposide) but not to other genotoxic agents including IR. However, this finding is compatible with recent studies linking SWI/SNF with TOP2A and TOP2BP1. Depletion of BRG1 and BRM did not result in genomic instability in a tumor-derived cell line but did result in nucleoplasmic bridges in normal human fibroblasts. Taken together, these results suggest that SWI/SNF tumor-suppressor activity involves a role in the DDR to attenuate replicative stress and genomic instability. These results may also help to inform the selection of chemotherapeutics for tumors deficient for SWI/SNF function.
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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.