ArticleMolecular and cellular biology2002
Cell cycle arrest and repression of cyclin D1 transcription by INI1/hSNF5.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.
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Who cites it
117 citing papers in PubMed, 230 citations in OpenAlex.
- SMARCB1-related schwannomatosis and other SMARCB1-associated phenotypes: clinical spectrum and molecular pathogenesis.Familial cancer · 2025Review
- Molecular Biomarkers of Glioma.Biomedicines · 2025Review
- AURKA/PLK1/CDC25C Axis as a Novel Therapeutic Target in INI1-Deficient Epithelioid Sarcoma.Cancer science · 2025Article
- Rhabdoid Tumor of the Kidney and Soft Tissues: Results from National Wilms Tumor Study-5 and Children's Oncology Group Study AREN0321.Pediatric blood & cancer · 2025Article
- Functional screening reveals genetic dependencies and diverging cell cycle control in atypical teratoid rhabdoid tumors.Genome biology · 2024Article
- A Case Study from the Past: "The RGC-5 vs. the 661W Cell Line: Similarities, Differences and Contradictions-Are They Really the Same?"International journal of molecular sciences · 2023Article
- Recent insights into the SWI/SNF complex and the molecular mechanism of hSNF5 deficiency in rhabdoid tumors.Cancer medicine · 2023Review
- Electric Fields Regulate In Vitro Surface Phosphatidylserine Exposure of Cancer Cells via a Calcium-Dependent Pathway.Biomedicines · 2023Article
- Inhibition of nuclear export restores nuclear localization and residual tumor suppressor function of truncated SMARCB1/INI1 protein in a molecular subset of atypical teratoid/rhabdoid tumors.Acta neuropathologica · 2021Article
- Human SNF5 arming of double-deleted vaccinia virus shows oncolytic and cytostatic activity against central nervous system atypical teratoid/rhabdoid tumor cells.Cancer gene therapy · 2021Article
- Review
- Article
- Understanding the trajectory of research efforts in atypical teratoid rhabdoid tumors: a bibliometric analysis of the 50 most impactful studies to date.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2021Article
- SMARCB1 Gene Mutation Predisposes to Earlier Development of Glioblastoma: A Case Report of Familial GBM.Journal of neuropathology and experimental neurology · 2020Article
- Characterization of molecular signatures of supratentorial ependymomas.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- SMARCB1 Promotes Ubiquitination and Degradation of NR4A3 via Direct Interaction Driven by ROS in Vascular Endothelial Cell Injury.Oxidative medicine and cellular longevity · 2020Article
- Article
- The Expression of Microvesicles in Leukemia: Prognostic Approaches.Cell journal · 2019Article
- Inhibition of MYC by the SMARCB1 tumor suppressor.Nature communications · 2019Article
- Polo-Like Kinase 4 (PLK4) Is Overexpressed in Central Nervous System Neuroblastoma (CNS-NB).Bioengineering (Basel, Switzerland) · 2018Article
57 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
INI1/hSNF5 is a component of the ATP-dependent chromatin remodeling hSWI/SNF complex and a tumor suppressor gene of aggressive pediatric atypical teratoid and malignant rhabdoid tumors (AT/RT). To understand the molecular mechanisms underlying its tumor suppressor function, we studied the effect of reintroduction of INI1/hSNF5 into AT/RT-derived cell lines such as MON that carry biallelic deletions of the INI1/hSNF5 locus. We demonstrate that expression of INI1/hSNF5 causes G(0)-G(1) arrest and flat cell formation in these cells. In addition, INI1/hSNF5 repressed transcription of cyclin D1 gene in MON, in a histone deacetylase (HDAC)-dependent manner. Chromatin immunoprecipitation studies revealed that INI1/hSNF5 was directly recruited to the cyclin D1 promoter and that its binding correlated with recruitment of HDAC1 and deacetylation of histones at the promoter. Analysis of INI1/hSNF5 truncations indicated that cyclin D1 repression and flat cell formation are tightly correlated. Coexpression of cyclin D1 from a heterologous promoter in MON was sufficient to eliminate the INI1-mediated flat cell formation and cell cycle arrest. Furthermore, cyclin D1 was overexpressed in AT/RT tumors. Our data suggest that one of the mechanisms by which INI1/hSNF5 exerts its tumor suppressor function is by mediating the cell cycle arrest due to the direct recruitment of HDAC activity to the cyclin D1 promoter thereby causing its repression and G(0)-G(1) arrest. Repression of cyclin D1 gene expression may serve as a useful strategy to treat AT/RT.
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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.