4.5 Article

LncRNA LINC00341 mediates PM2.5-induced cell cycle arrest in human bronchial epithelial cells

Journal

TOXICOLOGY LETTERS
Volume 276, Issue -, Pages 1-10

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.toxlet.2017.03.026

Keywords

PM2.5; LINC00341; Cell cycle arrest; G2/M phase; p21

Categories

Funding

  1. National Natural Science Foundation of China [91643204, 21277036, 81172633, 81473000]
  2. Key Program of Guangdong Natural Science Foundation [2014A030311017]
  3. University Major Program of Guangdong [2014SZD48, 2015KTSCX113]
  4. University Talent Program of Guangdong [2013-164]
  5. Science and Technology Program of Guangzhou, China [201607010013]

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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.

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