ArticleMolecular cancer2009
The chromatin remodelling factor BRG1 is a novel binding partner of the tumor suppressor p16INK4a.
Article in Molecular cancer, 2009. 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, 58 citations in OpenAlex.
- The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options.Molecular cancer · 2026Review
- Primary gastric SMARCA4-deficient carcinosarcoma and sarcomatoid carcinoma: Two case reports.Frontiers in oncology · 2025Article
- SWI/SNF Chromatin Remodeling Enzymes in Melanoma.Epigenomes · 2022Review
- Deubiquitination of MITF-M Regulates Melanocytes Proliferation and Apoptosis.Frontiers in molecular biosciences · 2021Article
- Remodeling the cancer epigenome: mutations in the SWI/SNF complex offer new therapeutic opportunities.Expert review of anticancer therapy · 2019Review
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- Brahma compensates the role of brahma-related gene 1 in liver regeneration ofInternational journal of clinical and experimental pathology · 2017Article
- Brahma-related gene 1 induces apoptosis in a p53-dependent manner in human rheumatoid fibroblast-like synoviocyte MH7A.Medicine · 2016Article
- HBP1-mediated Regulation of p21 Protein through the Mdm2/p53 and TCF4/EZH2 Pathways and Its Impact on Cell Senescence and Tumorigenesis.The Journal of biological chemistry · 2016Article
- Histone Modifications, Modifiers and Readers in Melanoma Resistance to Targeted and Immune Therapy.Cancers · 2015Review
- Combining BET and HDAC inhibitors synergistically induces apoptosis of melanoma and suppresses AKT and YAP signaling.Oncotarget · 2015Article
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- The epigenetic regulator I-BET151 induces BIM-dependent apoptosis and cell cycle arrest of human melanoma cells.The Journal of investigative dermatology · 2014Article
- Brg1 loss attenuates aberrant wnt-signalling and prevents wnt-dependent tumourigenesis in the murine small intestine.PLoS genetics · 2014Article
- Functional epigenetics approach identifies BRM/SMARCA2 as a critical synthetic lethal target in BRG1-deficient cancers.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- SWI/SNF chromatin remodeling enzymes in melanocyte differentiation and melanoma.Critical reviews in eukaryotic gene expression · 2014Review
- Beyond Mutations: Additional Mechanisms and Implications of SWI/SNF Complex Inactivation.Frontiers in oncology · 2014Review
- Multiple functions of Kip-related protein5 connect endoreduplication and cell elongation.Plant physiology · 2013Article
- MITF-independent pro-survival role of BRG1-containing SWI/SNF complex in melanoma cells.PloS one · 2013Article
- The chromatin remodeling and mRNA splicing functions of the Brahma (SWI/SNF) complex are mediated by the SNR1/SNF5 regulatory subunit.Nucleic acids research · 2012Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCDKN2A/p16INK4a is frequently altered in human cancers and it is the most important melanoma susceptibility gene identified to date. p16INK4a inhibits pRb phosphorylation and induces cell cycle arrest, which is considered its main tumour suppressor function. Nevertheless, additional activities may contribute to the tumour suppressor role of p16INK4a and could help explain its specific association with melanoma predisposition. To identify such functions we conducted a yeast-two-hybrid screen for novel p16INK4a binding partners.
resultsWe now report that p16INK4a interacts with the chromatin remodelling factor BRG1. We investigated the cooperative roles of p16INK4a and BRG1 using a panel of cell lines and a melanoma cell model with inducible p16INK4a expression and BRG1 silencing. We found evidence that BRG1 is not required for p16INK4a-induced cell cycle inhibition and propose that the p16INK4a-BRG1 complex regulates BRG1 chromatin remodelling activity. Importantly, we found frequent loss of BRG1 expression in primary and metastatic melanomas, implicating this novel p16INK4a binding partner as an important tumour suppressor in melanoma.
conclusionThis data adds to the increasing evidence implicating the SWI/SNF chromatin remodelling complex in tumour development and the association of p16INK4a with chromatin remodelling highlights potentially new functions that may be important in melanoma predisposition and chemoresistance.
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