ArticleThe Journal of biological chemistry2012
Polycomb (PcG) proteins, BMI1 and SUZ12, regulate arsenic-induced cell transformation.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 39 citations in OpenAlex.
- Effect of Gentianella acuta (Michx.) Hulten against the arsenic-induced development hindrance of mouse oocytes.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Article
- The expression and role of SUZ12 in lung adenocarcinoma.Cancer medicine · 2024Article
- Review
- Arsenic-induced epigenetic changes in cancer development.Seminars in cancer biology · 2021Review
- Molecular Mechanisms of Arsenic-Induced Disruption of DNA Repair.Chemical research in toxicology · 2020Review
- Ubiquitin-specific protease 3 promotes cell migration and invasion by interacting with and deubiquitinating SUZ12 in gastric cancer.Journal of experimental & clinical cancer research : CR · 2019Article
- Arsenite malignantly transforms human prostate epithelial cells in vitro by gene amplification of mutated KRAS.PloS one · 2019Article
- Intrauterine multi-metal exposure is associated with reduced fetal growth through modulation of the placental gene network.Environment international · 2018Article
- Prognostic implications of polycomb proteins ezh2, suz12, and eed1 and histone modification by H3K27me3 in sarcoma.BMC cancer · 2018Article
- Polycomb Repressor Complex 2 in Genomic Instability and Cancer.International journal of molecular sciences · 2017Review
- Influence of Arsenic on Global Levels of Histone Posttranslational Modifications: a Review of the Literature and Challenges in the Field.Current environmental health reports · 2016Review
- p38α MAPK is required for arsenic-induced cell transformation.Molecular carcinogenesis · 2016Article
- Potential roles of EZH2, Bmi-1 and miR-203 in cell proliferation and invasion in hepatocellular carcinoma cell line Hep3B.World journal of gastroenterology · 2015Article
- Polycomb Group (PcG) Proteins and Human Cancers: Multifaceted Functions and Therapeutic Implications.Medicinal research reviews · 2015Review
- E2F1-mediated FOS induction in arsenic trioxide-induced cellular transformation: effects of global H3K9 hypoacetylation and promoter-specific hyperacetylation in vitro.Environmental health perspectives · 2015Article
- Bidirectional functions of arsenic as a carcinogen and an anti-cancer agent in human squamous cell carcinoma.PloS one · 2014Article
- Long-term effects of chromatin remodeling and DNA damage in stem cells induced by environmental and dietary agents.Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer · 2013Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Inorganic arsenic is a well-documented human carcinogen associated with cancers of the skin, lung, liver, and bladder. However, the underlying mechanisms explaining the tumorigenic role of arsenic are not well understood. The present study explored a potential mechanism of cell transformation induced by arsenic exposure. Exposure to a low dose (0.5 μm) of arsenic trioxide (As(2)O(3)) caused transformation of BALB/c 3T3 cells. In addition, in a xenograft mouse model, tumor growth of the arsenic-induced transformed cells was dramatically increased. In arsenic-induced transformed cells, polycomb group (PcG) proteins, including BMI1 and SUZ12, were activated resulting in enhanced histone H3K27 tri-methylation levels. On the other hand, tumor suppressor p16(INK4a) and p19(ARF) mRNA and protein expression were dramatically suppressed. Introduction of small hairpin (sh) RNA-BMI1 or -SUZ12 into BALB/c 3T3 cells resulted in suppression of arsenic-induced transformation. Histone H3K27 tri-methylation returned to normal in BMI1- or SUZ12-knockdown BALB/c 3T3 cells compared with BMI1- or SUZ12-wildtype cells after arsenic exposure. As a consequence, the expression of p16(INK4a) and p19(ARF) was recovered in arsenic-treated BMI1- or SUZ12-knockdown cells. Thus, arsenic-induced cell transformation was blocked by inhibition of PcG function. Taken together, these results strongly suggest that the polycomb proteins, BMI1 and SUZ12 are required for cell transformation induced by organic arsenic exposure.
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