Effects of arsenic exposure on DNA methylation and epigenetic gene regulation.
Effects of arsenic exposure on DNA methylation and epigenetic gene regulation.
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作者：
Reichard JF;Puga A
砷是一种非致突变的人类致癌物，通过未知的机制诱导肿瘤。越来越多的证据表明其致癌性来自表观遗传变化，特别是DNA甲基化。砷介导的基因甲基化状态的变化，已经被提出激活癌基因表达或沉默肿瘤抑制基因，导致控制细胞转化的基因活性的长期变化。大多数描述性的，往往是矛盾的，研究表明，砷暴露与低和高甲基化在体内或体外的各种基因位点。这种模糊性使得难以评估砷诱导的变化是否与转化过程有因果关系，或者仅仅是快速分裂的癌细胞生理学改变的反映。在这里，我们讨论了支持DNA甲基化变化作为砷致癌原因的证据，并强调了这些研究的优势和局限性，以及存在差异和不一致的领域。
Arsenic is a nonmutagenic human carcinogen that induces tumors through unknown mechanisms. A growing body of evidence suggests that its carcinogenicity results from epigenetic changes, particularly in DNA methylation. Changes in gene methylation status, mediated by arsenic, have been proposed activate oncogene expression or silence tumor suppressor genes, leading to long-term changes in activity of genes controlling cell transformation. Mostly descriptive, and often contradictory, studies have demonstrated that arsenic exposure is associated with both hypo- and hyper-methylation at various genetic loci in vivo or in vitro. This ambiguity has made it difficult to assess whether the changes induced by arsenic are causally involved in the transformation process or are simply a reflection of the altered physiology of rapidly dividing cancer cells. Here, we discuss the evidence supporting changes in DNA methylation as a cause of arsenic carcinogenesis and highlight the strengths and limitations of these studies, as well areas where consistencies and inconsistencies exist.
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DOI：
10.1006/bbrc.1993.1750
发表时间：
1993-06-30
影响因子：
3.1
作者：
BALAGHI, M;WAGNER, C
通讯作者：
WAGNER, C
影响因子：
4.8
作者：
Coppin, Jean-Francois;Qu, Wei;Waalkes, Michael P.
通讯作者：
Waalkes, Michael P.
影响因子：
3.8
作者：
Chen, H;Liu, J;Waalkes, MP
通讯作者：
Waalkes, MP
影响因子：
6.4
作者：
Chen, W-T;Hung, W-C;Chai, C-Y
通讯作者：
Chai, C-Y
影响因子：
3.5
作者：
Bestor, TH
通讯作者：
Bestor, TH