ArticleCell cycle (Georgetown, Tex.)2012
Epigenetic inactivation of the tumor suppressor BIN1 drives proliferation of SNF5-deficient tumors.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- BIN1 in cancer: biomarker and therapeutic target.Journal of cancer research and clinical oncology · 2023Review
- Advances in Therapeutic Targeting of Cancer Stem Cells within the Tumor Microenvironment: An Updated Review.Cells · 2020Review
- Trial watch: IDO inhibitors in cancer therapy.Oncoimmunology · 2020Review
- microRNA-21 Aggravates Lipopolysaccharide-Induced Inflammation in MH7A Cells Through Targeting SNF5.Inflammation · 2020Article
- Partitioning of MLX-Family Transcription Factors to Lipid Droplets Regulates Metabolic Gene Expression.Molecular cell · 2020Article
- Inflammatory Reprogramming with IDO1 Inhibitors: Turning Immunologically Unresponsive 'Cold' Tumors 'Hot'.Trends in cancer · 2018Review
- Indoleamine 2,3-Dioxygenase and Its Therapeutic Inhibition in Cancer.International review of cell and molecular biology · 2018Review
- Discovery of IDO1 Inhibitors: From Bench to Bedside.Cancer research · 2017Review
- Indoleamine 2,3-dioxygenase pathways of pathogenic inflammation and immune escape in cancer.Cancer immunology, immunotherapy : CII · 2014Review
- Cytoplasmic interaction of the tumour suppressor protein hSNF5 with dynamin-2 controls endocytosis.Oncogene · 2014Article
- The histone deacetylase inhibitor SAHA acts in synergism with fenretinide and doxorubicin to control growth of rhabdoid tumor cells.BMC cancer · 2013Article
- Durable tumor regression in genetically altered malignant rhabdoid tumors by inhibition of methyltransferase EZH2.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Rhabdoid tumors: an initial clue to the role of chromatin remodeling in cancer.Brain pathology (Zurich, Switzerland) · 2013Review
- SNF5 reexpression in malignant rhabdoid tumors regulates transcription of target genes by recruitment of SWI/SNF complexes and RNAPII to the transcription start site of their promoters.Molecular cancer research : MCR · 2013Article
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
Abstract
Emerging evidence demonstrates that subunits of the SWI/SNF chromatin remodeling complex are specifically mutated at high frequency in a variety of human cancer types. SNF5 (SMARCB1/INI1/BAF47), a core subunit of the SWI/SNF complex, is inactivated in the vast majority of rhabdoid tumors (RT), an aggressive type of pediatric cancer. SNF5-deficient cancers are diploid and genomically stable, suggesting that epigenetically based changes in transcription are key drivers of tumor formation caused by SNF5 loss. However, there is limited understanding of the target genes that drive cancer formation following SNF5 loss. Here we performed comparative expression analyses upon three independent SNF5-deficient cancer data sets from both human and mouse and identify downregulation of the BIN1 tumor suppressor as a conserved event in primary SNF5-deficient cancers. We show that SNF5 recruits the SWI/SNF complex to the BIN1 promoter, and that the marked reduction of BIN1 expression in RT correlates with decreased SWI/SNF occupancy. Functionally, we demonstrate that re-expression of BIN1 specifically compromises the proliferation of SNF5-deficient RT cell lines. Identification of BIN1 as a SNF5 target gene reveals a novel tumor suppressive regulatory mechanism whose disruption can drive cancer formation.
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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.