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首页> 外文期刊>Particle Fibre Toxicology >Ambient PM exposure and DNA methylation in tumor suppressor genes: a cross-sectional study
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Ambient PM exposure and DNA methylation in tumor suppressor genes: a cross-sectional study

机译：抑癌基因中环境性PM暴露和DNA甲基化的横断面研究

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Exposure to ambient air particles matter (PM) has been associated with increased risk of lung cancer. Aberrant tumor suppressor gene promoter methylation has emerged as a promising biomarker for cancers, including lung cancer. Whether exposure to PM is associated with peripheral blood leukocyte (PBL) DNA methylation in tumor suppressor genes has not been evaluated. In 63 male healthy steel workers with well-characterized exposure to metal-rich particles nearby Brescia, Italy, we evaluated whether exposure to PM and metal components was associated with PBL DNA methylation in 4 tumor suppressor genes (i.e., APC, p16, p53 and RASSF1A). Blood samples were obtained on the 1st (baseline) and 4th day (post-exposure) of the same work week and DNA methylation was measured using pyrosequencing. A linear mixed model was used to examine the correlations of the exposure with promoter methylation levels. Mean promoter DNA methylation levels of APC or p16 were significantly higher in post-exposure samples compared to that in baseline samples (p-values = 0.005 for APC, and p-value = 0.006 for p16). By contrast, the mean levels of p53 or RASSF1A promoter methylation was decreased in post-exposure samples compared to that in baseline samples ( p-value = 0.015 for p53; and p-value 10 (β = 0.27, 95% CI: 0.13-0.40), and PM1 (β = 0.23, 95% CI: 0.09-0.38). In summary, ambient PM exposure was associated with PBL DNA methylation levels of tumor suppressor genes of APC, p16, p53 and RASSF1A, suggesting that such methylation alterations may reflect processes related to PM-induced lung carcinogenesis.
机译：暴露于环境空气中的颗粒物（PM）与患肺癌的风险增加有关。异常的肿瘤抑制基因启动子甲基化已成为包括肺癌在内的癌症的有前途的生物标志物。是否暴露于PM是否与肿瘤抑制基因中的外周血白细胞（PBL）DNA甲基化有关，尚未进行评估。在意大利布雷西亚附近的63名男性健康钢铁工人中，特征性地暴露于富含金属的颗粒中，我们评估了PM和金属成分的暴露是否与4种抑癌基因（即APC，p16，p53和RASSF1A）。在第1 st （基线）和第4 （在相同工作周的暴露时间），并使用焦磷酸测序法测量DNA甲基化程度。使用线性混合模型检查暴露与启动子甲基化水平的相关性。与基线样品相比，暴露后样品中APC或p16的平均启动子DNA甲基化水平显着更高（APC的p值= 0.005，p16的p值= 0.006）。相比之下，与基线样品相比，暴露后样品中p53或RASSF1A启动子甲基化的平均水平降低（p53的p值= 0.015; p值为10 （β= 0.27，95％ CI：0.13-0.40）和PM 1 （β= 0.23，95％CI：0.09-0.38）。总而言之，环境PM暴露与PBL相关APC，p16，p53和RASSF1A抑癌基因的DNA甲基化水平表明这种甲基化改变可能反映了与PM诱导的肺癌发生有关的过程。

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