LncRNA LINC00341 mediates PM-induced cell cycle arrest in human bronchial epithelial cells.

Toxicol Lett

State Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou 511436, PR China. Electronic address:

Published: July 2017

Fine particulate matter (PM) 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 PM on cell cycle progression in human bronchial epithelial cells (16HBE) and the underlying mechanism mediated by lncRNAs. PM treatment inhibited cell proliferation in 16HBE cells in a dose-dependent manner. The results of flow cytometry assay (FCM) showed that PM induced cell apoptosis and cell cycle arrest at G2/M phase. The lncRNA microarray analysis indicated that treatment with PM 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 PM treatment. Further functional studies showed that knockdown of lncRNA LINC00341 reversed PM-induced G2/M phase cell cycle arrest and p21 expression. These results suggest that up-regulation of the lncRNA LINC00341 mediates PM-induced cell cycle arrest at the G2/M phase, and probably through regulating the expression of p21.

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http://dx.doi.org/10.1016/j.toxlet.2017.03.026DOI Listing

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