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

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

Markey Cancer Center / Cancer Research Priority Initiative

Research output: Contribution to journal › Article › peer-review

35 Scopus citations

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.

Original language	English
Pages (from-to)	1-10
Number of pages	10
Journal	Toxicology Letters
Volume	276
DOIs	https://doi.org/10.1016/j.toxlet.2017.03.026
State	Published - Jul 5 2017

Bibliographical note

Publisher Copyright:
© 2017 Elsevier B.V.

Keywords

Cell cycle arrest
G2/M phase
LINC00341
PM
p21

ASJC Scopus subject areas

Toxicology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.toxlet.2017.03.026

Cite this

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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 PM2.5 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.",

keywords = "Cell cycle arrest, G2/M phase, LINC00341, PM, p21",

author = "Yiqin Xu and Jianjun Wu and Xiaowu Peng and Ti Yang and Meiling Liu and Lijian Chen and Xin Dai and Zhishan Wang and Chengfeng Yang and Bing Yan and Yiguo Jiang",

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T1 - LncRNA LINC00341 mediates PM2.5-induced cell cycle arrest in human bronchial epithelial cells

AU - Xu, Yiqin

AU - Wu, Jianjun

AU - Peng, Xiaowu

AU - Yang, Ti

AU - Liu, Meiling

AU - Chen, Lijian

AU - Dai, Xin

AU - Wang, Zhishan

AU - Yang, Chengfeng

AU - Yan, Bing

AU - Jiang, Yiguo

PY - 2017/7/5

Y1 - 2017/7/5

N2 - 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.

AB - 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.

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KW - G2/M phase

KW - LINC00341

KW - PM

KW - p21

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