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LncRNA LINC00341 mediates PM2.5-induced cell cycle arrest in human bronchial epithelial cells
Yiqin Xu1, Jianjun Wu1, Xiaowu Peng2
1State Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou 511436, PR China.
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.
Insights
Fine particulate matter (PM2.5) triggers cell cycle arrest and apoptosis in lung cells. This study reveals that the lncRNA LINC00341 mediates these effects by regulating p21 expression, clarifying a key pathogenic mechanism.
Area of Science:
- Environmental Health
- Molecular Biology
- Cell Biology
Background:
- Fine particulate matter (PM2.5) exposure is linked to respiratory diseases, but its pathogenic mechanisms are not fully understood.
- Understanding how PM2.5 affects cellular processes is crucial for developing preventative strategies.
Purpose of the Study:
- To investigate the impact of PM2.5 on cell cycle progression in human bronchial epithelial cells (16HBE).
- To elucidate the role of long non-coding RNAs (lncRNAs) in mediating PM2.5-induced cellular damage.
Main Methods:
- Human bronchial epithelial cells (16HBE) were treated with PM2.5.
- Cell proliferation, apoptosis, and cell cycle distribution were analyzed using flow cytometry.
- lncRNA expression profiles were assessed via microarray analysis, with differential expression confirmed by qRT-PCR.
- Functional studies involved knockdown of specific lncRNAs to determine their role in PM2.5 effects.
Main Results:
- PM2.5 inhibited 16HBE cell proliferation in a dose-dependent manner.
- PM2.5 induced apoptosis and cell cycle arrest at the G2/M phase.
- lncRNA expression profiles were significantly altered by PM2.5 exposure.
- lncRNA LINC00341 was notably upregulated and its knockdown reversed PM2.5-induced G2/M arrest and p21 expression.
Conclusions:
- PM2.5 exposure disrupts normal cell cycle progression in bronchial epithelial cells.
- The lncRNA LINC00341 plays a critical role in mediating PM2.5-induced G2/M phase cell cycle arrest.
- Upregulation of LINC00341 likely contributes to PM2.5 pathogenesis by regulating p21 expression.