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

Yiqin Xu; Jianjun Wu; Xiaowu Peng; Ti Yang; Meiling Liu; Lijian Chen; Xin Dai; Zhishan Wang; Chengfeng Yang; Bing Yan; Yiguo Jiang

doi:10.1016/j.toxlet.2017.03.026

LncRNA LINC00341 mediates PM_2.5-induced cell cycle arrest in human bronchial epithelial cells

Toxicol Lett. 2017 Jul 5:276:1-10. doi: 10.1016/j.toxlet.2017.03.026. Epub 2017 Mar 31.

Authors

Yiqin Xu¹, Jianjun Wu², Xiaowu Peng³, Ti Yang¹, Meiling Liu¹, Lijian Chen¹, Xin Dai¹, Zhishan Wang⁴, Chengfeng Yang⁴, Bing Yan⁵, Yiguo Jiang⁶

Affiliations

¹ State Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou 511436, PR China.
² State Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou 511436, PR China. Electronic address: wooland@126.com.
³ Center for Environmental Health Research, South China Institute of Environmental Sciences, Ministry of Environmental Protection, Guangzhou 510655, PR China.
⁴ Department of Toxicology and Cancer Biology, Center for Research on Environmental Disease, College of Medicine, University of Kentucky, Lexington, KY 40536, USA.
⁵ School of Chemistry and Chemical Engineering, Shandong University, Jinan, 250100, PR China.
⁶ State Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou 511436, PR China. Electronic address: jiangyiguo@vip.163.com.

PMID: 28366736
DOI: 10.1016/j.toxlet.2017.03.026

Abstract

Fine particulate matter (PM_2.5) 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 PM_2.5 on cell cycle progression in human bronchial epithelial cells (16HBE) and the underlying mechanism mediated by lncRNAs. PM_2.5 treatment inhibited cell proliferation in 16HBE cells in a dose-dependent manner. The results of flow cytometry assay (FCM) showed that PM_2.5 induced cell apoptosis and cell cycle arrest at G2/M phase. The lncRNA microarray analysis indicated that treatment with PM_2.5 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 PM_2.5 treatment. Further functional studies showed that knockdown of lncRNA LINC00341 reversed PM_2.5-induced G2/M phase cell cycle arrest and p21 expression. These results suggest that up-regulation of the lncRNA LINC00341 mediates PM_2.5-induced cell cycle arrest at the G2/M phase, and probably through regulating the expression of p21.

Keywords: Cell cycle arrest; G2/M phase; LINC00341; PM(2.5); p21.

MeSH terms

Apoptosis / drug effects
Bronchi / drug effects*
Bronchi / metabolism
Bronchi / pathology
Cell Line, Transformed
Cell Proliferation / drug effects*
Cyclin-Dependent Kinase Inhibitor p21 / metabolism
Dose-Response Relationship, Drug
Epithelial Cells / drug effects*
Epithelial Cells / metabolism
Epithelial Cells / pathology
Flow Cytometry
G2 Phase Cell Cycle Checkpoints / drug effects*
Gene Expression Profiling / methods
Humans
Oligonucleotide Array Sequence Analysis
Particle Size
Particulate Matter / toxicity*
RNA Interference
RNA, Long Noncoding / genetics
RNA, Long Noncoding / metabolism*
Real-Time Polymerase Chain Reaction
Transfection
Up-Regulation

Substances

CDKN1A protein, human
Cyclin-Dependent Kinase Inhibitor p21
Particulate Matter
RNA, Long Noncoding
long non-coding RNA LINC00341, human