抑制 miR-32 的活性可通过调节肺癌细胞中 Smad1 介导的信号通路促进 PM2.5 暴露诱导的 EMT。
Inhibition of miR-32 activity promoted EMT induced by PM2.5 exposure through the modulation of the Smad1-mediated signaling pathways in lung cancer cells.
机构信息
Key Laboratory of Environmental Pollution and Microecology of Liaoning Province, Shenyang Medical College, No. 146, North Huanghe Street, Huanggu District, Shenyang City, 110034, PR China; Department of Pharmacology, Shenyang Medical College, No. 146, North Huanghe Street, Huanggu District, Shenyang City, 110034, PR China.
Key Laboratory of Environmental Pollution and Microecology of Liaoning Province, Shenyang Medical College, No. 146, North Huanghe Street, Huanggu District, Shenyang City, 110034, PR China; Department of Toxicology, School of Public Health, Shenyang Medical College, No. 146, North Huanghe Street, Huanggu District, Shenyang City, 110034, PR China.
出版信息
Chemosphere. 2017 Oct;184:289-298. doi: 10.1016/j.chemosphere.2017.05.152. Epub 2017 May 30.
Epithelial mesenchymal transition (EMT) is a crucial morphological event during tumor progression. The present study reported that EMT could be triggered by airborne fine particulate matter (PM) with a mean diameter of less than 2.5 μm (PM2.5) in human lung cancer cells. We also aimed to elucidate the possible mechanisms of these processes. The results showed that treatment with PM2.5 promoted the activity of the SMAD family member 1 (Smad1)-mediated signaling pathway and downregulated the expression of the inhibitory Smad proteins Smad6 and Smad7 in lung cancer cells. Moreover, the knockdown of Smad1 suppressed the EMT process induced by PM2.5 exposure. Our data further revealed that miR-32 has a negative effect on PM2.5-induced EMT. The results showed that the expression level of miR-32 was significantly upregulated in the PM2.5-induced EMT process. The knockdown of miR-32 enhances the activity of the Smad1-mediated signaling pathway, which promotes the EMT process induced by PM2.5. Thus, these findings indicate that PM2.5 can induce the EMT process through the Smad1-mediated signaling pathway, and miR-32 may act as an EMT inhibitor in lung cancer cells.
上皮间质转化（EMT）是肿瘤进展过程中的一个重要形态事件。本研究报道，空气中直径小于 2.5μm 的细颗粒物（PM2.5）可引发人肺癌细胞 EMT。我们还旨在阐明这些过程的可能机制。结果表明，PM2.5 处理可促进 SMAD 家族成员 1（Smad1）介导的信号通路的活性，并下调肺癌细胞中抑制性 Smad 蛋白 Smad6 和 Smad7 的表达。此外，Smad1 的敲低可抑制 PM2.5 暴露诱导的 EMT 过程。我们的数据进一步表明，miR-32 对 PM2.5 诱导的 EMT 具有负向作用。结果表明，miR-32 在 PM2.5 诱导的 EMT 过程中的表达水平显著上调。miR-32 的敲低增强了 Smad1 介导的信号通路的活性，从而促进了 PM2.5 诱导的 EMT 过程。因此，这些发现表明 PM2.5 可以通过 Smad1 介导的信号通路诱导 EMT 过程，而 miR-32 可能在肺癌细胞中作为 EMT 抑制剂发挥作用。
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