title: LncRNA LINC00341 mediates PM2.5-induced cell cycle arrest in human bronchial epithelial cells.
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 PM2.5on cell cycle progression in human bronchial epithelial cells (16HBE) and the underlying mechanism mediated by lncRNAs. PM2.5treatment inhibited cell proliferation in 16HBE cells in a dose-dependent manner. The results of flow cytometry assay (FCM) showed that PM2.5induced cell apoptosis and cell cycle arrest at G2/M phase. The lncRNA microarray analysis indicated that treatment with PM2.5led 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 PM2.5treatment. 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.
authors.affiliation: State Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou 511436, PR China.
authors.forename: Yiqin
authors.initials: Y
authors.lastname: Xu
authors.affiliation: State Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou 511436, PR China. Electronic address: wooland@126.com.
authors.forename: Jianjun
authors.initials: J
authors.lastname: Wu
authors.affiliation: Center for Environmental Health Research, South China Institute of Environmental Sciences, Ministry of Environmental Protection, Guangzhou 510655, PR China.
authors.forename: Xiaowu
authors.initials: X
authors.lastname: Peng
authors.affiliation: State Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou 511436, PR China.
authors.forename: Ti
authors.initials: T
authors.lastname: Yang
authors.affiliation: State Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou 511436, PR China.
authors.forename: Meiling
authors.initials: M
authors.lastname: Liu
authors.affiliation: State Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou 511436, PR China.
authors.forename: Lijian
authors.initials: L
authors.lastname: Chen
authors.affiliation: State Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou 511436, PR China.
authors.forename: Xin
authors.initials: X
authors.lastname: Dai
authors.affiliation: Department of Toxicology and Cancer Biology, Center for Research on Environmental Disease, College of Medicine, University of Kentucky, Lexington, KY 40536, USA.
authors.forename: Zhishan
authors.initials: Z
authors.lastname: Wang
authors.affiliation: Department of Toxicology and Cancer Biology, Center for Research on Environmental Disease, College of Medicine, University of Kentucky, Lexington, KY 40536, USA.
authors.forename: Chengfeng
authors.initials: C
authors.lastname: Yang
authors.affiliation: School of Chemistry and Chemical Engineering, Shandong University, Jinan, 250100, PR China.
authors.forename: Bing
authors.initials: B
authors.lastname: Yan
authors.affiliation: State Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou 511436, PR China. Electronic address: jiangyiguo@vip.163.com.
authors.forename: Yiguo
authors.initials: Y
authors.lastname: Jiang
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D001980:Bronchi / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D002461:Cell Line, Transformed; D049109:Cell Proliferation / Q000187:drug effects*; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D005434:Flow Cytometry; D059565:G2 Phase Cell Cycle Checkpoints / Q000187:drug effects*; D020869:Gene Expression Profiling / Q000379:methods; D006801:Humans; D020411:Oligonucleotide Array Sequence Analysis; D010316:Particle Size; D052638:Particulate Matter / Q000633:toxicity*; D034622:RNA Interference; D062085:RNA, Long Noncoding / Q000235:genetics / Q000378:metabolism*; D060888:Real-Time Polymerase Chain Reaction; D014162:Transfection; D015854:Up-Regulation
chemical_list: C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D052638:Particulate Matter; D062085:RNA, Long Noncoding; C000621675:long non-coding RNA LINC00341, human
keywords: Cell cycle arrest; G2/M phase; LINC00341; PM(2.5); p21