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Genes 2013, 4(4), 583-595;

Nickel and Epigenetic Gene Silencing

Department of Environmental Medicine, NYU School of Medicine, Tuxedo, NY 10987, USA
Department of Environmental Sciences, Faculty of Meteorology, Environment and Arid Land Agriculture, King Abdulaziz University, Jeddah 21589, Saudi Arabia
Author to whom correspondence should be addressed.
Received: 21 May 2013 / Revised: 11 October 2013 / Accepted: 17 October 2013 / Published: 25 October 2013
(This article belongs to the Special Issue Gene Silencing)
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Insoluble nickel compounds are well-established human carcinogens. Occupational exposure to these compounds leads to increased incidence of lung and nasal cancer in nickel refinery workers. Apart from its weak mutagenic activity and hypoxia mimicking effect there is mounting experimental evidence indicating that epigenetic alteration plays an important role in nickel-induced carcinogenesis. Multiple epigenetic mechanisms have been identified to mediate nickel-induced gene silencing. Nickel ion is able to induce heterochromatinization by binding to DNA-histone complexes and initiating chromatin condensation. The enzymes required for establishing or removing epigenetic marks can be targeted by nickel, leading to altered DNA methylation and histone modification landscapes. The current review will focus on the epigenetic changes that contribute to nickel-induced gene silencing. View Full-Text
Keywords: epigenetics; gene silencing; heterochromatin; DNA methylation; histone modification; miRNA epigenetics; gene silencing; heterochromatin; DNA methylation; histone modification; miRNA

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Sun, H.; Shamy, M.; Costa, M. Nickel and Epigenetic Gene Silencing. Genes 2013, 4, 583-595.

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