ArticleMolecular and cellular biology2008
Loss of the epigenetic tumor suppressor SNF5 leads to cancer without genomic instability.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 120 citations in OpenAlex.
- PHIP suppresses NuRD to enable the growth of SWI/SNF-mutant cancers.Nature communications · 2026Article
- Epigenetic targeting of PGBD5-dependent DNA damage in SMARCB1-deficient sarcomas.The Journal of clinical investigation · 2025Article
- MYC Regulates a DNA Repair Gene Expression Program in Small Cell Carcinoma of the Ovary, Hypercalcemic Type.Cancers · 2025Article
- Overcoming Clinical Resistance to EZH2 Inhibition Using Rational Epigenetic Combination Therapy.Cancer discovery · 2024Article
- The IL6/JAK/STAT3 signaling axis is a therapeutic vulnerability in SMARCB1-deficient bladder cancer.Nature communications · 2024Article
- Article
- The role of chromatin remodeler SMARCA4/BRG1 in brain cancers: a potential therapeutic target.Oncogene · 2023Review
- SMARCB1 Loss in Poorly Differentiated Chordomas Drives Tumor Progression.The American journal of pathology · 2023Article
- Molecular targeted therapies for pediatric atypical teratoid/rhabdoid tumors.Pediatric investigation · 2022Review
- Mechanisms of the synergistic lung tumorigenic effect of arsenic and benzo(a)pyrene combined- exposure.Seminars in cancer biology · 2021Review
- Epigenetic regulation of cancer stem cell formation and maintenance.International journal of cancer · 2021Review
- Metal carcinogen exposure induces cancer stem cell-like property through epigenetic reprograming: A novel mechanism of metal carcinogenesis.Seminars in cancer biology · 2019Review
- Case-based review: atypical teratoid/rhabdoid tumor.Neuro-oncology practice · 2019Review
- Remodeling the cancer epigenome: mutations in the SWI/SNF complex offer new therapeutic opportunities.Expert review of anticancer therapy · 2019Review
- Atypical Teratoid Rhabdoid Tumour : From Tumours to Therapies.Journal of Korean Neurosurgical Society · 2018Review
- Disruption of mammalian SWI/SNF and polycomb complexes in human sarcomas: mechanisms and therapeutic opportunities.The Journal of pathology · 2018Review
- Chromatin remodeler CHD1 promotes XPC-to-TFIIH handover of nucleosomal UV lesions in nucleotide excision repair.The EMBO journal · 2017Article
- SMARCB1 is required for widespread BAF complex-mediated activation of enhancers and bivalent promoters.Nature genetics · 2017Article
- Prognostic factors and survival in non-central nervous system rhabdoid tumors.Journal of pediatric surgery · 2017Article
- Smarca4 ATPase mutations disrupt direct eviction of PRC1 from chromatin.Nature genetics · 2017Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
There is a growing appreciation of the role that epigenetic alterations can play in oncogenesis. However, given the large number of genetic anomalies present in most cancers, it has been difficult to evaluate the extent to which epigenetic changes contribute to cancer. SNF5 (INI1/SMARCB1/BAF47) is a tumor suppressor that regulates the epigenome as a core member of the SWI/SNF chromatin remodeling complex. While the SWI/SNF complex displays potent tumor suppressor activity, it is unknown whether this activity is exerted genetically via maintenance of genome integrity or epigenetically via transcriptional regulation. Here we show that Snf5-deficient primary cells do not show altered sensitivity to DNA damaging agents, defects in gamma-H2AX induction, or an abrogated DNA damage checkpoint. Further, the aggressive malignancies that arise following SNF5 loss are diploid and genomically stable. Remarkably, we demonstrate that most human SNF5-deficient cancers lack genomic amplifications/deletions and, aside from SNF5 loss, are indistinguishable from normal cells on single-nucleotide polymorphism arrays. Finally, we show that epigenetically based changes in transcription that occur following SNF5 loss correlate with the tumor phenotype. Collectively, our results provide novel insight into the mechanisms of oncogenesis by demonstrating that disruption of a chromatin remodeling complex can largely, if not completely, substitute for genomic instability in the genesis of aggressive cancer.
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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.