Chanda Sarmishtha, Dasgupta Uma B, Guhamazumder Debendranath, Gupta Mausumi, Chaudhuri Utpal, Lahiri Sarbari, Das Subhankar, Ghosh Nilima, Chatterjee Debdutta
Department of Biophysics, Molecular Biology and Genetics, University of Calcutta, 92, APC Road, Kolkata- 700009, India.
Toxicol Sci. 2006 Feb;89(2):431-7. doi: 10.1093/toxsci/kfj030. Epub 2005 Oct 26.
Chronic arsenic exposure is known to produce arsenicosis and cancer. To ascertain whether perturbation of methylation plays a role in such carcinogenesis, the degree of methylation of p53 and p16 gene in DNA obtained from blood samples of people chronically exposed to arsenic and skin cancer subjects was studied. Methylation-specific restriction endonuclease digestion followed by polymerase chain reaction (PCR) of gene p53 and bisulfite treatment followed by methylation-sensitive PCR of gene p16 have been carried out to analyze the methylation status of the samples studied. Significant DNA hypermethylation of promoter region of p53 gene was observed in DNA of arsenic-exposed people compared to control subjects. This hypermethylation showed a dose-response relationship. Further, hypermethylation of p53 gene was also observed in arsenic-induced skin cancer patients compared to subjects having skin cancer unrelated to arsenic, though not at significant level. However, a small subgroup of cases showed hypomethylation with high arsenic exposure. Significant hypermethylation of gene p16 was also observed in cases of arsenicosis exposed to high level of arsenic. In man, arsenic has the ability to alter DNA methylation patterns in gene p53 and p16, which are important in carcinogenesis.
已知长期接触砷会导致砷中毒和癌症。为确定甲基化紊乱是否在此类致癌过程中起作用,对长期接触砷者的血液样本及皮肤癌患者样本中的p53和p16基因的甲基化程度进行了研究。采用甲基化特异性限制性内切酶消化后进行p53基因的聚合酶链反应(PCR),以及亚硫酸氢盐处理后进行p16基因的甲基化敏感PCR,以分析所研究样本的甲基化状态。与对照受试者相比,在接触砷者的DNA中观察到p53基因启动子区域显著的DNA高甲基化。这种高甲基化呈现剂量反应关系。此外,与非砷相关皮肤癌患者相比,在砷诱导的皮肤癌患者中也观察到p53基因的高甲基化,尽管差异不显著。然而,一小部分病例在高砷暴露情况下显示低甲基化。在高砷暴露的砷中毒病例中也观察到p16基因显著的高甲基化。在人类中,砷能够改变p53和p16基因的DNA甲基化模式,而这两个基因在致癌过程中很重要。