ArticleToxicology and applied pharmacology2010
Arsenite induced poly(ADP-ribosyl)ation of tumor suppressor P53 in human skin keratinocytes as a possible mechanism for carcinogenesis associated with arsenic exposure.
Article in Toxicology and applied pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 48 citations in OpenAlex.
- Mode of action-based risk assessment of genotoxic carcinogens.Archives of toxicology · 2020Review
- NEnvironmental pollution (Barking, Essex : 1987) · 2020Article
- The Role of Reactive Oxygen Species in Arsenic Toxicity.Biomolecules · 2020Review
- Akt Regulated Phosphorylation of GSK-3β/Cyclin D1, p21 and p27 Contributes to Cell Proliferation Through Cell Cycle Progression From G1 to S/G2M Phase in Low-Dose Arsenite Exposed HaCat Cells.Frontiers in pharmacology · 2019Article
- PARP1-produced poly-ADP-ribose causes the PARP12 translocation to stress granules and impairment of Golgi complex functions.Scientific reports · 2017Article
- Oncogenomic disruptions in arsenic-induced carcinogenesis.Oncotarget · 2017Review
- Low-dose dose-response for reduced cell viability after exposure of human keratinocyte (HEK001) cells to arsenite.Toxicology reports · 2017Article
- MicroRNA-21 activation of AktToxicology research · 2016Article
- Arsenic Disruption of DNA Damage Responses-Potential Role in Carcinogenesis and Chemotherapy.Biomolecules · 2015Review
- Synergistic cytotoxicity and DNA strand breaks in cells and plasmid DNA exposed to uranyl acetate and ultraviolet radiation.Journal of applied toxicology : JAT · 2015Article
- Nicotinamide enhances repair of arsenic and ultraviolet radiation-induced DNA damage in HaCaT keratinocytes and ex vivo human skin.PloS one · 2015Article
- Molecular features in arsenic-induced lung tumors.Molecular cancer · 2013Review
- Sodium arsenite ± hyperthermia sensitizes p53-expressing human ovarian cancer cells to cisplatin by modulating platinum-DNA damage responses.Toxicological sciences : an official journal of the Society of Toxicology · 2012Article
- Interdependent genotoxic mechanisms of monomethylarsonous acid: role of ROS-induced DNA damage and poly(ADP-ribose) polymerase-1 inhibition in the malignant transformation of urothelial cells.Toxicology and applied pharmacology · 2011Article
- Concentration-dependent cellular responses of arsenic in keratinocytes.The Kaohsiung journal of medical sciences · 2011Review
- Reply to "Reversal and prevention of arsenic-induced human bronchial epithelial cell malignant transformation by microRNA-200b".Toxicological sciences : an official journal of the Society of Toxicology · 2011Article
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2 authors.
Funding
Abstract
Arsenite is an environmental pollutant. Exposure to inorganic arsenic in drinking water is associated with elevated cancer risk, especially in skin. Arsenite alone does not cause skin cancer in animals, but arsenite can enhance the carcinogenicity of solar UV. Arsenite is not a significant mutagen at non-toxic concentrations, but it enhances the mutagenicity of other carcinogens. The tumor suppressor protein P53 and nuclear enzyme PARP-1 are both key players in DNA damage response. This laboratory demonstrated earlier that in cells treated with arsenite, the P53-dependent increase in p21(WAF1/CIP1) expression, normally a block to cell cycle progression after DNA damage, is deficient. Here we show that although long-term exposure of human keratinocytes (HaCaT) to a nontoxic concentration (0.1 microM) of arsenite decreases the level of global protein poly(ADP-ribosyl)ation, it increases poly(ADP-ribosyl)ation of P53 protein and PARP-1 protein abundance. We also demonstrate that exposure to 0.1 microM arsenite depresses the constitutive expression of p21 mRNA and P21 protein in HaCaT cells. Poly(ADP-ribosyl)ation of P53 is reported to block its activation, DNA binding and its functioning as a transcription factor. Our results suggest that arsenite's interference with activation of P53 via poly(ADP-ribosyl)ation may play a role in the comutagenic and cocarcinogenic effects of arsenite.
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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.