ArticleMolecular cancer research : MCR2013
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.
Article in Molecular cancer research : MCR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Role of epigenetics in paediatric cancer pathogenesis & drug resistance.British journal of cancer · 2025Review
- Recent insights into the SWI/SNF complex and the molecular mechanism of hSNF5 deficiency in rhabdoid tumors.Cancer medicine · 2023Review
- RUNX1-Survivin Axis Is a Novel Therapeutic Target for Malignant Rhabdoid Tumors.Molecules and cells · 2022Article
- Dual targeting of EZH1 and EZH2 for the treatment of malignant rhabdoid tumors.Molecular therapy oncolytics · 2022Article
- A Role for SMARCB1 in Synovial Sarcomagenesis Reveals That SS18-SSX Induces Canonical BAF Destruction.Cancer discovery · 2021Article
- Global Chromatin Changes Resulting from Single-Gene Inactivation-The Role of SMARCB1 in Malignant Rhabdoid Tumor.Cancers · 2021Article
- MDM2 and MDM4 Are Therapeutic Vulnerabilities in Malignant Rhabdoid Tumors.Cancer research · 2019Article
- The chromatin remodeler ZmCHB101 impacts alternative splicing contexts in response to osmotic stress.Plant cell reports · 2019Article
- Expression and potential role of SNF5 in endometrial carcinoma.BMC women's health · 2019Article
- Loss of Snf5 Induces Formation of an Aberrant SWI/SNF Complex.Cell reports · 2017Article
- The molecular pathogenesis of schwannomatosis, a paradigm for the co-involvement of multiple tumour suppressor genes in tumorigenesis.Human genetics · 2017Review
- Review
- Coordinating cell proliferation and differentiation: Antagonism between cell cycle regulators and cell type-specific gene expression.Cell cycle (Georgetown, Tex.) · 2016Review
- Generation of a mouse model of atypical teratoid/rhabdoid tumor of the central nervous system through combined deletion of Snf5 and p53.Cancer research · 2015Article
- FOXP1 potentiates Wnt/β-catenin signaling in diffuse large B cell lymphoma.Science signaling · 2015Article
- SNF5/INI1 deficiency redefines chromatin remodeling complex composition during tumor development.Molecular cancer research : MCR · 2014Article
- Mechanisms by which SMARCB1 loss drives rhabdoid tumor growth.Cancer genetics · 2014Review
- SWI/SNF chromatin remodeling complexes and cancer.American journal of medical genetics. Part C, Seminars in medical genetics · 2014Review
- Gene silencing associated with SWI/SNF complex loss during NSCLC development.Molecular cancer research : MCR · 2014Article
- Article
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4 authors at 2 institutions in 2 countries.
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Abstract
Malignant rhabdoid tumor (MRT), a highly aggressive cancer of young children, displays inactivation or loss of the hSNF5/INI1/SMARCB1 gene, a core subunit of the SWI/SNF chromatin-remodeling complex, in primary tumors and cell lines. We have previously reported that reexpression of hSNF5 in some MRT cell lines causes a G1 arrest via p21(CIP1/WAF1) (p21) mRNA induction in a p53-independent manner. However, the mechanism(s) by which hSNF5 reexpression activates gene transcription remains unclear. We initially searched for other hSNF5 target genes by asking whether hSNF5 loss altered regulation of other consensus p53 target genes. Our studies show that hSNF5 regulates only a subset of p53 target genes, including p21 and NOXA, in MRT cell lines. We also show that hSNF5 reexpression modulates SWI/SNF complex levels at the transcription start site (TSS) at both loci and leads to activation of transcription initiation through recruitment of RNA polymerase II (RNAPII) accompanied by H3K4 and H3K36 modifications. Furthermore, our results show lower NOXA expression in MRT cell lines compared with other human tumor cell lines, suggesting that hSNF5 loss may alter the expression of this important apoptotic gene. Thus, one mechanism for MRT development after hSNF5 loss may rely on reduced chromatin-remodeling activity of the SWI/SNF complex at the TSS of critical gene promoters. Furthermore, because we observe growth inhibition after NOXA expression in MRT cells, the NOXA pathway may provide a novel target with clinical relevancy for treatment of this aggressive disease.
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