LncRNA LINC00341 mediates PM2.5-induced cell cycle arrest in human bronchial epithelial cells. (5th July 2017)

• Record Type: Journal Article
• Authors: Xu, Yiqin; Wu, Jianjun; Peng, Xiaowu; Yang, Ti; Liu, Meiling; Chen, Lijian; Dai, Xin; Wang, Zhishan; Yang, Chengfeng; Yan, Bing; Jiang, Yiguo
• Is Part Of: Toxicology letters. Volume 276(2017)
• Page Start: 1
• Page End: 10
• Publication Date: 2017-07-05
• Subjects: PM2.5 -- LINC00341 -- Cell cycle arrest -- G2/M phase -- p21; Toxicology -- Periodicals; 363.179
• DOI: 10.1016/j.toxlet.2017.03.026
• Languages: English
• ISSNs: 0378-4274

Abstract

Graphical abstract: Highlights: PM2.5 exposure could induce the alteration of lncRNA expression profiles. LINC00341 was upregulated expression and could mediate cell cycle arrest at G2/M phase. LINC00341 may modulate the PM2.5 -induced cell cycle arrest by regulating the expression of p21. Abstract: 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. lncRNA 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.