摘要
Epidemiological studies have demonstrated that fine particulate matter（PM（2.5）） exposure causes airway inflammation, which may lead to lung cancer. The activation of epithelial–mesenchymal transition（EMT） is assumed to be a crucial step in lung tumor metastasis and development. We assessed the EMT effect of low concentrations（0, 0.1, 1.0, and 5.0 μg/m L）of PM（2.5） organic extract on a human bronchial epithelial cell line（BEAS-2 B）. PM（2.5） samples were collected from three cities（Shanghai, Ningbo, and Nanjing） in the Yangtze River Delta（YRD） region in autumn 2014. BEAS-2 B cells were exposed to the PM（2.5） extract to assess cell viability, invasion ability as well as the relative m RNA and protein expressions of EMT markers. Our findings revealed that BEAS-2 B cells changed from the epithelial to mesenchymal phenotype after exposure. In all groups, PM（2.5） exposure dose-dependently decreased the expression of E-cadherin and increased the expression of Vimentin. The key transcription factors, including ZEB1 and Slug, were significantly up-regulated upon exposure. These results indicated that the PM（2.5） organic extract induced different degrees of EMT progression in BEAS-2 B cells. The cell invasion ability increased in a concentration-dependent manner after 48 hr of treatment with the extract. This study offers a novel insight into the effects of PM（2.5） on EMT and the potential health risks associated with PM（2.5） in the YRD region.
Epidemiological studies have demonstrated that fine particulate matter（PM（2.5）） exposure causes airway inflammation, which may lead to lung cancer. The activation of epithelial–mesenchymal transition（EMT） is assumed to be a crucial step in lung tumor metastasis and development. We assessed the EMT effect of low concentrations（0, 0.1, 1.0, and 5.0 μg/m L）of PM（2.5） organic extract on a human bronchial epithelial cell line（BEAS-2 B）. PM（2.5） samples were collected from three cities（Shanghai, Ningbo, and Nanjing） in the Yangtze River Delta（YRD） region in autumn 2014. BEAS-2 B cells were exposed to the PM（2.5） extract to assess cell viability, invasion ability as well as the relative m RNA and protein expressions of EMT markers. Our findings revealed that BEAS-2 B cells changed from the epithelial to mesenchymal phenotype after exposure. In all groups, PM（2.5） exposure dose-dependently decreased the expression of E-cadherin and increased the expression of Vimentin. The key transcription factors, including ZEB1 and Slug, were significantly up-regulated upon exposure. These results indicated that the PM（2.5） organic extract induced different degrees of EMT progression in BEAS-2 B cells. The cell invasion ability increased in a concentration-dependent manner after 48 hr of treatment with the extract. This study offers a novel insight into the effects of PM（2.5） on EMT and the potential health risks associated with PM（2.5） in the YRD region.
基金
supported by the National Natural Science Foundation of China (Nos. 41390240, 21477124, 21677140, 21477123 and 21507128)
the Knowledge Innovation Program of the Chinese Academy of Sciences (Nos. IUEMS201405,IUEQN201506)
the Science and Technology Program of Fujian Province (No. 2016 T3005)
the grant from Xiamen Municipal Bureau of Science and Technology Program (No. 3502Z20161236)
