LncRNA LINC00341 mediates PM2.5-induced cell cycle arrest in human bronchial epithelial cells
LncRNA LINC00341 mediates PM2.5-induced cell cycle arrest in human bronchial epithelial cells
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LncRNA LINC00341 介导 PM2.5 诱导的人支气管上皮细胞细胞周期停滞
DOI：
10.1016/j.toxlet.2017.03.026
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发表时间：
2017-07-05
影响因子：
3.5
通讯作者：
Jiang, Yiguo
中科院分区：
文献类型：
--
作者：
Xu, Yiqin;Wu, Jianjun;Jiang, Yiguo
细颗粒物（PM2.5）可粘附多种有毒物质，引发呼吸道疾病，但其致病机制尚不清楚。在本研究中，我们研究了 PM2.5 对人支气管上皮细胞 (16HBE) 细胞周期进程的影响以及 lncRNA 介导的潜在机制。 PM2.5处理以剂量依赖性方式抑制16HBE细胞的细胞增殖。流式细胞术(FCM)结果显示PM2.5诱导细胞凋亡和细胞周期停滞在G2/M期。 lncRNA 微阵列分析表明，PM2.5 处理导致 lncRNA 表达谱发生改变。进行 qRT-PCR 来确认几种候选 lncRNA 的差异表达。 PM2.5处理后16HBE细胞中IncRNA LINC00341显着上调。进一步的功能研究表明，lncRNA LINC00341 的敲低可逆转 PM2.5 诱导的 G2/M 期细胞周期停滞和 p21 表达。这些结果表明，lncRNA LINC00341 的上调介导 PM2.5 诱导的细胞周期停滞在 G2/M 期，并且可能是通过调节 p21 的表达来实现的。
Fine particulate matter (PM2.5) could adhere to many toxic substances and cause respiratory diseases.However, the associated pathogenic mechanism remains unclear. In this study, we investigated the effects of PM2.5 on cell cycle progression in human bronchial epithelial cells (16HBE) and the underlying mechanism mediated by lncRNAs. PM2.5 treatment inhibited cell proliferation in 16HBE cells in a dose-dependent manner. The results of flow cytometry assay (FCM) showed that PM2.5 induced cell apoptosis and cell cycle arrest at G2/M phase. The lncRNA microarray analysis indicated that treatment with PM2.5 led to the alteration of lncRNA expression profiles. qRT-PCR were performed to confirm the differential expression of several candidate lncRNAs. IncRNA LINC00341 was significantly up-regulated in 16HBE cell after PM2.5 treatment. Further functional studies showed that knockdown of lncRNA LINC00341 reversed PM2.5-induced G2/M phase cell cycle arrest and p21 expression. These results suggest that up-regulation of the lncRNA LINC00341 mediates PM2.5-induced cell cycle arrest at the G2/M phase, and probably through regulating the expression of p21.