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首页> 外文期刊>Journal of Environmental Radioactivity >Human lung epithelial cells cultured in the presence of radon-emitting rock experience gene expression changes similar to those associated with tobacco smoke exposure
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Human lung epithelial cells cultured in the presence of radon-emitting rock experience gene expression changes similar to those associated with tobacco smoke exposure

机译：在发射ra气的岩石中培养的人肺上皮细胞的基因表达变化类似于与烟草烟雾暴露相关的基因表达变化

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摘要

Radon is the second leading cause of lung cancer, after tobacco smoke. While tobacco smoke-induced carcinogenesis has been studied extensively, far less is known about radon-induced carcinogenesis, particularly in relation to the influence of radon on gene expression. The objectives of the work described herein were to (a) determine if and how exposure to low dose radon-emitting rock influences cells, at the gene expression level, and (b) compare any gene expression changes resulting from the exposure to radon-emitting rock with those induced by exposure to tobacco smoke. Any potential radiation-induced gene expression changes were also compared to those induced by exposure to cannabis smoke, a non-carcinogen at low doses, used here as a smoke exposure comparator. Human lung epithelial cells were exposed to radon-emitting rock, tobacco smoke or cannabis smoke, over months, and RNA-sequencing was carried out. We found that the rock-exposed cells experienced significant gene expression changes, particularly of the geneAKR1C3, and that these changes, over time, increasingly reflected those associated with exposure to tobacco, but not cannabis, smoke. We postulate that the early gene expression changes common to both the radiation and tobacco smoke exposures constitute a related - potentially pre-carcinogenic - response. Our findings suggest that the length of time a dividing population of cells is exposed to a constant low concentration of radon (with a potential cumulative absorbed dose) could be an important risk parameter for neoplastic transformation/carcinogenesis.
机译：tobacco是仅次于烟草烟雾的第二大肺癌诱因。尽管已经广泛研究了烟草烟雾诱导的致癌作用，但对ra诱导的致癌作用的了解还很少，特别是在ra对基因表达的影响方面。本文所述工作的目的是（a）确定在基因表达水平上低剂量ra发射岩石的暴露是否以及如何影响细胞，以及（b）比较因暴露于emitting发射导致的任何基因表达变化岩石与暴露于烟草烟雾引起的岩石。还将任何可能的辐射诱导基因表达变化与通过暴露于低剂量非致癌物大麻烟（在此用作烟暴露比较剂）诱导的基因表达变化进行了比较。将人肺上皮细胞暴露于散发ra气的岩石，烟草烟雾或大麻烟雾中，历时数月，然后进行了RNA测序。我们发现暴露于岩石的细胞经历了显着的基因表达变化，特别是geneAKR1C3的基因表达变化，并且随着时间的推移，这些变化越来越多地反映出与暴露于烟草（而不是大麻）烟雾相关的那些表达。我们假设辐射和烟草烟雾暴露共同的早期基因表达变化构成了相关的潜在潜在的致癌反应。我们的研究结果表明，分裂细胞群体暴露于恒定低浓度low（具有潜在的累积吸收剂量）的时间长度可能是肿瘤转化/致癌作用的重要风险参数。

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