ArticleCancer research2010
Reexpression of hSNF5 in malignant rhabdoid tumor cell lines causes cell cycle arrest through a p21(CIP1/WAF1)-dependent mechanism.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- Combined inhibition of BETs and HDACs as a potential epigenetics-based therapy for malignant rhabdoid tumor.Cell death & disease · 2026Article
- SMARCB1-related schwannomatosis and other SMARCB1-associated phenotypes: clinical spectrum and molecular pathogenesis.Familial cancer · 2025Review
- Chromatin remodeling and cancer: the critical influence of the SWI/SNF complex.Epigenetics & chromatin · 2025Review
- Recent insights into the SWI/SNF complex and the molecular mechanism of hSNF5 deficiency in rhabdoid tumors.Cancer medicine · 2023Review
- Dual targeting of EZH1 and EZH2 for the treatment of malignant rhabdoid tumors.Molecular therapy oncolytics · 2022Article
- Nobiletin downregulates the SKP2-p21/p27-CDK2 axis to inhibit tumor progression and shows synergistic effects with palbociclib on renal cell carcinoma.Cancer biology & medicine · 2021Article
- Loss of SWI/SNF Chromatin Remodeling Alters NRF2 Signaling in Non-Small Cell Lung Carcinoma.Molecular cancer research : MCR · 2020Article
- SMARCB1 Acts as a Quiescent Gatekeeper for Cell Cycle and Immune Response in Human Cells.International journal of molecular sciences · 2020Article
- Small-Molecule and CRISPR Screening Converge to Reveal Receptor Tyrosine Kinase Dependencies in Pediatric Rhabdoid Tumors.Cell reports · 2019Article
- MDM2 and MDM4 Are Therapeutic Vulnerabilities in Malignant Rhabdoid Tumors.Cancer research · 2019Article
- Expression and potential role of SNF5 in endometrial carcinoma.BMC women's health · 2019Article
- CDK 4/6 Inhibitors as Single Agent in Advanced Solid Tumors.Frontiers in oncology · 2018Review
- Evaluation of the role of downregulation of SNF5/INI1 core subunit of SWI/SNF complex in clear cell renal cell carcinoma development.American journal of cancer research · 2017Article
- MYC interaction with the tumor suppressive SWI/SNF complex member INI1 regulates transcription and cellular transformation.Cell cycle (Georgetown, Tex.) · 2016Article
- Coordinating cell proliferation and differentiation: Antagonism between cell cycle regulators and cell type-specific gene expression.Cell cycle (Georgetown, Tex.) · 2016Review
- LIN28B is highly expressed in atypical teratoid/rhabdoid tumor (AT/RT) and suppressed through the restoration of SMARCB1.Cancer cell international · 2016Article
- Genome-wide methylome analyses reveal novel epigenetic regulation patterns in schizophrenia and bipolar disorder.BioMed research international · 2015Article
- BRG1/SMARCA4 inactivation promotes non-small cell lung cancer aggressiveness by altering chromatin organization.Cancer research · 2014Article
- SNF5/INI1 deficiency redefines chromatin remodeling complex composition during tumor development.Molecular cancer research : MCR · 2014Article
- Vulnerabilities of mutant SWI/SNF complexes in cancer.Cancer cell · 2014Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Loss of hSNF5 function is usually observed in malignant rhabdoid tumor (MRT), a highly aggressive pediatric neoplasm. Previous studies have shown that reexpression of hSNF5 in MRT cell lines causes G1 cell cycle arrest with p16(INK4A), p21(CIP1/WAF1), and cyclin D1 playing key roles in MRT cell growth control. However, we have shown that reexpression of hSNF5 induced cell cycle arrest in the absence of p16(INK4A) expression. These results indicate that the mechanism of hSNF5-induced cell cycle arrest is context dependent. Here, we investigated the relationship between p21(CIP1/WAF1) and hSNF5 in the regulation of growth using several MRT cell lines. We found that G1 cell cycle arrest occurred concomitant with an increase in p21(CIP1/WAF1) mRNA and protein levels and preceded p16(INK4A) mRNA and protein upregulation. Chromatin immunoprecipitation data confirmed that hSNF5 appeared at both p21(CIP1/WAF1) and p16(INK4A) promoters after reexpression. We further showed that p21(CIP1/WAF1) induction showed both p53-dependent and p53-independent mechanisms. We also showed that reduction of p21(CIP1/WAF1) expression by RNAi significantly inhibited hSNF5-induced G(1) arrest. Our results show that both p21(CIP1/WAF1) and p16(INK4A) are targets for hSNF5 and that p21(CIP1/WAF1) upregulation during hSNF5-induced G(1) arrest precedes p16(INK4A) upregulation. These findings indicate that SNF5 mediates a temporally controlled program of cyclin-dependent kinase inhibition to restrict aberrant proliferation in MRT cells.
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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.