期刊
ONCOTARGET
卷 7, 期 23, 页码 35026-35043出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.9019
关键词
PM2.5; microRNA; lung cancer; carcinogenesis; actin
资金
- National Natural Science Foundation of China [81472938, 81572495]
- Fund of the Distinguished Talents of Jiangsu Province [BK20150021]
- Natural Science Foundation of Jiangsu Province [BK20151418]
- fund of the Distinguished Professor of Jiangsu Province
- Fundamental Research Funds for the Central Universities
Recent studies have linked ambient fine particulate matter (PM2.5) to increased lung cancer mortality and morbidity. However, the underlying mechanism causing the adverse effects of PM2.5 is less clear. In the present study, post-transcriptional profiling was used to explore biological pathways involved in PM2.5-induced pulmonary disorders. The carcinogenesis and metastasis of PM2.5 exposure were evaluated by long-term PM2.5 exposure tests. We observed dysregulation of actin in A549 cells line and dysplasia in the lungs of mice exposed to PM2.5. Both PM2.5-exposed cells and animals showed increased Rnd3 expression levels. Moreover, miR-802 mimics rescued actin disorganization in vitro and alveolitis in vivo. Long-term exposure to PM2.5 promoted carcinogenesis and metastasis of pulmonary cells. Decreased miR-802 expression levels in the serum samples of PM2.5-treated mice and individuals from moderately polluted cities were observed. Increased Rnd3 expression levels in lung cancers tissues have been identified by a genome database TCGA, and have been linked to less overall survival probabilities of lung cancer patients. Our findings suggest that dysregulation of actin cytoskeleton and down-regulation of miR-802 expression might be the underlying mechanism involved in the adverse effects of PM2.5 exposure. In addition, long-term exposure to PM2.5 demonstrated strong associations with malignant pulmonary disorders.
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