Effects of nickel, chromate, and arsenite on histone 3 lysine methylation.
Effects of nickel, chromate, and arsenite on histone 3 lysine methylation.
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DOI：
10.1016/j.taap.2009.01.009
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发表时间：
2009-04-01
影响因子：
3.8
通讯作者：
Costa M
中科院分区：
文献类型：
--
作者：
Zhou X;Li Q;Arita A;Sun H;Costa M
职业暴露于含镍（Ni）、铬（Cr）和砷（As）的化合物与肺癌和其他不良健康影响有关。它们的致癌特性可能部分归因于DNA甲基化状态和组蛋白尾翻译后修饰的变化诱导的基因表达的激活和/或抑制。在这里，我们表明，镍，铬酸盐和亚砷酸盐的个人治疗都影响基因激活标记H3K4甲基化。我们发现镍（1 mM）、铬酸盐（10 μ M）和亚砷酸盐（1 μ M）在人肺癌A549细胞中暴露24 h后显著增加三甲基H3K4。暴露于较低水平的镍（50和100 μ M）、铬酸盐（0.5和1 μ M）或亚砷酸盐（0.1、0.5和1 μ M）7天也增加了A549细胞中的三甲基化H3K4。在去除1 μ M亚砷酸盐后7天，该标记仍然保持升高并通过细胞分裂遗传。我们还通过双染色免疫荧光显微镜证实，在A549细胞中，暴露于每种金属处理24小时后，H3K4三甲基和H3K9二甲基标记均整体增加。然而，三甲基H3K4和二甲基H3K9标记定位于细胞核中的不同区域。因此，我们的研究提供了进一步的证据，即镍、铬酸盐和亚砷酸盐金属化合物的致癌性机制可能涉及各种组蛋白尾部修饰的改变，这些改变反过来可能影响可能引起转化的基因的表达。
Occupational exposure to nickel(Ni), chromium(Cr), and arsenic(As) containing compounds has been associated with lung cancer and other adverse health effects. Their carcinogenic properties may be attributable in part, to activation and/or repression of gene expression induced by changes in the DNA methylation status and histone tail post-translational modifications. Here we show that individual treatment with nickel, chromate, and arsenite all affect the gene activating mark H3K4 methylation. We found that nickel(1 mM), chromate(10 μM), and arsenite(1 μM) significantly increase tri-methyl H3K4 after 24 h exposure in human lung carcinoma A549 cells. Seven days of exposure to lower levels of nickel(50 and 100 μM), chromate(0.5 and 1 μM) or arsenite(0.1 0.5 and 1 μM) also increased tri-methylated H3K4 in A549 cells. This mark still remained elevated and inherited through cell division seven days following removal of 1 μM arsenite. We also demonstrate by dual staining immunofluorescence microscopy that both H3K4 tri-methyl and H3K9 di-methyl marks increase globally after 24 h exposure to each metal treatment in A549 cells. However, the tri-methyl H3K4 and di-methyl H3K9 marks localize in different regions in the nucleus of the cell. Thus, our study provides further evidence that a mechanism(s) of carcinogenicity of nickel, chromate, and arsenite metal compounds may involve alterations of various histone tail modifications that may in turn affect the expression of genes that may cause transformation.
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