ArticleScientific reports2019
SMARCA2-deficiency confers sensitivity to targeted inhibition of SMARCA4 in esophageal squamous cell carcinoma cell lines.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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
23 citing papers in PubMed, 50 citations in OpenAlex.
- The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options.Molecular cancer · 2026Review
- Implications for clinical prognosis and target discovery of the SWI/SNF complex in genitourinary tumors.Discover oncology · 2026Review
- Advances in epigenetic therapy for esophageal cancer.Clinical epigenetics · 2026Review
- Long non-coding RNA UCA1 modulates SMARCA2-containing SWI/SNF chromatin remodeling complexes in human colorectal cancer.iScience · 2026Article
- SMARCA2 is an essential and potent cofactor for a specific subset of the glucocorticoid response in A549 cells.bioRxiv : the preprint server for biology · 2025Article
- Proteomic compensation by paralogs preserves protein interaction networks after gene loss in cancer.Molecular systems biology · 2025Article
- Discovery of Pyrimidoindolones as Novel Family VIII Bromodomain Binders.ACS medicinal chemistry letters · 2025Article
- TARGET-SL: precision essential gene prediction using driver prioritisation and synthetic lethality.Briefings in bioinformatics · 2025Article
- Synthetic lethal strategies for the development of cancer therapeutics.Nature reviews. Clinical oncology · 2025Review
- Chromatin remodellers as therapeutic targets.Nature reviews. Drug discovery · 2024Review
- Pharmacological targeting of the cancer epigenome.Nature cancer · 2024Review
- Review
- Mechanism of action of the SWI/SNF family complexes.Nucleus (Austin, Tex.) · 2023Article
- Alanine supplementation exploits glutamine dependency induced by SMARCA4/2-loss.Nature communications · 2023Article
- Synthetic lethality prediction in DNA damage repair, chromatin remodeling and the cell cycle using multi-omics data from cell lines and patients.Scientific reports · 2023Article
- SynLeGG: analysis and visualization of multiomics data for discovery of cancer 'Achilles Heels' and gene function relationships.Nucleic acids research · 2021Article
- Exploiting vulnerabilities of SWI/SNF chromatin remodelling complexes for cancer therapy.Oncogene · 2021Review
- SWI/SNF Alterations in Squamous Bladder Cancers.Genes · 2020Article
- The Intersection between Oral Microbiota, Host Gene Methylation and Patient Outcomes in Head and Neck Squamous Cell Carcinoma.Cancers · 2020Article
- Functional characterization of SMARCA4 variants identified by targeted exome-sequencing of 131,668 cancer patients.Nature communications · 2020Article
Corrections and comments
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Authors and funding
22 authors at 3 institutions in 2 countries.
Funding
Abstract
SMARCA4/BRG1 and SMARCA2/BRM, the two mutually exclusive catalytic subunits of the BAF complex, display a well-established synthetic lethal relationship in SMARCA4-deficient cancers. Using CRISPR-Cas9 screening, we identify SMARCA4 as a novel dependency in SMARCA2-deficient esophageal squamous cell carcinoma (ESCC) models, reciprocal to the known synthetic lethal interaction. Restoration of SMARCA2 expression alleviates the dependency on SMARCA4, while engineered loss of SMARCA2 renders ESCC models vulnerable to concomitant depletion of SMARCA4. Dependency on SMARCA4 is linked to its ATPase activity, but not to bromodomain function. We highlight the relevance of SMARCA4 as a drug target in esophageal cancer using an engineered ESCC cell model harboring a SMARCA4 allele amenable to targeted proteolysis and identify SMARCA4-dependent cell models with low or absent SMARCA2 expression from additional tumor types. These findings expand the concept of SMARCA2/SMARCA4 paralog dependency and suggest that pharmacological inhibition of SMARCA4 represents a novel therapeutic opportunity for SMARCA2-deficient cancers.
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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.