Biao Yang1, Xinming Li2, Dongmei Chen2, Chunling Xiao3. 1. Liaoning University of Traditional Chinese Medicine, Shenyang, Liaoning 110032, PR China. 2. Key Lab of Environmental Pollution and Microecology, Shenyang Medical College, Shenyang, Liaoning 110034, PR China. 3. Key Lab of Environmental Pollution and Microecology, Shenyang Medical College, Shenyang, Liaoning 110034, PR China. Electronic address: xiaochunling2000@126.com.
Abstract
PURPOSE: Airborne particulate matter smaller than 2.5μm (PM2.5) has been shown to induce adverse health effects through various mechanisms. However, its effects on gene expression in non-small-cell lung cancer (NSCLC) remain undefined. The aim of this study was to analyze the expression profile of PM2.5-induced adverse health effects on human. MATERIALS AND METHODS: We performed RNA sequencing to elucidate key molecular effects of PM2.5 collected from Shenyang China, to identify potential diagnostic markers or therapeutic targets, and further validated these differences in gene expression by using quantitative PCR in A549 and H1299 human non-small-cell lung cancer cell lines. To investigate the functional changes on PM2.5 exposed cells, we carried out the viability assay for the cell counting, and the Boyden chamber assay for invasion. RESULTS: We found 143 genes that were expressed at least twice as much, or no more than half as much, in NSCLC cells exposed to PM2.5 than in unexposed cells. Results showed deregulated genes confronted PM2.5 exposure were significantly expressed, but commonly expressed in NSCLC cells. In addition, according to the viability assay and the Boyden chamber assay, PM2.5 exposed cells which have more competent on proliferation and invasion can keep the line with the results in RNA-Seq. CONCLUSION: Our data may provide a more specific understanding of the signaling patterns associated with pathogenesis, and lead to novel markers and therapeutic targets for NSCLC.
PURPOSE: Airborne particulate matter smaller than 2.5μm (PM2.5) has been shown to induce adverse health effects through various mechanisms. However, its effects on gene expression in non-small-cell lung cancer (NSCLC) remain undefined. The aim of this study was to analyze the expression profile of PM2.5-induced adverse health effects on human. MATERIALS AND METHODS: We performed RNA sequencing to elucidate key molecular effects of PM2.5 collected from Shenyang China, to identify potential diagnostic markers or therapeutic targets, and further validated these differences in gene expression by using quantitative PCR in A549 and H1299 human non-small-cell lung cancer cell lines. To investigate the functional changes on PM2.5 exposed cells, we carried out the viability assay for the cell counting, and the Boyden chamber assay for invasion. RESULTS: We found 143 genes that were expressed at least twice as much, or no more than half as much, in NSCLC cells exposed to PM2.5 than in unexposed cells. Results showed deregulated genes confronted PM2.5 exposure were significantly expressed, but commonly expressed in NSCLC cells. In addition, according to the viability assay and the Boyden chamber assay, PM2.5 exposed cells which have more competent on proliferation and invasion can keep the line with the results in RNA-Seq. CONCLUSION: Our data may provide a more specific understanding of the signaling patterns associated with pathogenesis, and lead to novel markers and therapeutic targets for NSCLC.