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PM2.5长期暴露诱导人肺支气管上皮细胞恶性转化的研究
作者:费高强1  李伟2  葛尤1  卫斐然3 
单位:1. 东南大学 公共卫生学院, 江苏 南京 210009;
2. 南京医科大学附属儿童医院 质量管理办公室, 江苏 南京 210009;
3. 东南大学附属中大医院 风湿免疫科, 江苏 南京 210009
关键词:细颗粒物 肺支气管上皮细胞 恶性转化 
分类号:R122
出版年·卷·期(页码):2021·49·第十一期(1303-1306)
摘要:

目的:研究PM2.5长期暴露诱导人肺支气管上皮细胞(16HBE细胞)恶性转化的能力。方法:使用100μg·ml-1的PM2.5连续长期暴露16HBE细胞,并设立对照组。采用CCK-8法测定细胞增殖能力,EdU法检测细胞增殖活性,Transwell法评价细胞迁移与侵袭能力,集落形成实验检测细胞克隆形成能力。结果:CCK-8结果显示PM2.5长期暴露后的16HBE细胞增殖能力较对照组显著增强(P<0.01),随着暴露代数增加,细胞增殖能力逐渐升高;EdU结果提示PM2.5长期暴露后细胞的活性显著提升(P<0.001);与对照组相比,PM2.5暴露可显著增强16HBE细胞的迁移、侵袭及克隆形成能力(P<0.01)。结论:经PM2.5长期诱导的16HBE细胞可逐渐恶性转化。

Objective: To study the malignant transformation ability of human pulmonary bronchial epithelial cells (16HBE cells)induced by fine particulate matter (PM2.5) long-term exposure.Methods: 16HBE cells were continuously exposed to 100 μg·ml-1 PM2.5 for a long time, and control group was set up. Cell proliferation was measured by CCK-8 method, cell proliferation activity was measured by EdU method, cell migration and invasion ability were evaluated by Transwell method, and cell clonal formation ability was detected by clonal formation assay.Results:CCK-8 showed that the proliferation of 16HBE cells increased significantly after PM2.5 long-term exposure compared with the control group (P<0.01), and the proliferation of 16HBE cells in treatment group increased gradually with the increase of passage number. EdU results showed that the activity of cells in treatment group increased significantly after long-term exposure of PM2.5 (P<0.001). Compared with the control group, PM2.5 exposure significantly enhanced the migration, invasion and clonal formation of 16HBE cells (P<0.01). Conclusions:16HBE cells induced by PM2.5 for a long time can be transformed into malignant cells gradually.

参考文献:

[1] HAMRA G B,GUHA N,COHEN A,et al.Outdoor particulate matter exposure and lung cancer:a systematic review and meta-analysis[J].Environ Health Perspect,2014,122(9):906-911.
[2] ZHU X M,WANG Q,XING W W,et al.PM2.5 induces autophagy-mediated cell death via NOS2 signaling in human bronchial epithelium cells[J].Int J Bio Sci,2018,14(5):557-564.
[3] BOCCHI C,BAZZINI C,FONTANA F,et al.Characterization of urban aerosol:seasonal variation of mutagenicity and genotoxicity of PM(2.5),PM(1) and semi-volatile organic compounds[J].Mutat Res Genet Toxicol Environ Mutagen,2016,809:16-23.
[4] HUANG F,PAN B,WU J,et al.Relationship between exposure to PM2.5 and lung cancer incidence and mortality:a meta-analysis[J].Oncotarget,2017,8(26):43322-43331.
[5] GREENLEE R T,HILL-HARMON M B,MURRAY T,et al.Cancer statistics,2001[J].CA Cancer J Clin,2001,51(1):15-36.
[6] DUAN S,YUAN H,YU S,et al.Epigenetic-based biomarkers in the malignant transformation of beas-2b cells induced by coal tar pitch extract[J].Medicina (Kaunas),2020,57(1):24.
[7] LI R,ZHOU R,ZHANG J.Function of PM2.5 in the pathogenesis of lung cancer and chronic airway inflammatory diseases[J].Oncol Lett,2018,15(5):7506-7514.
[8] LOOMIS D,GROSSE Y,LAUBY-SECRETAN B,et al.The carcinogenicity of outdoor air pollution[J].Lancet Oncol,2013,14(13):1262-1263.
[9] BAI L,SHIN S,BURNETT R T,et al.Exposure to ambient air pollution and the incidence of lung cancer and breast cancer in the Ontario population health and environment cohort[J].Int J Cancer,2020,146(9):2450-2459.
[10] SOMBOONSIN P,CANUDAS-ROMO V.Mortality attributable to fine particulate matter in Asia,2000-2015:a cross-sectional cause-of-death analysis[J].BMJ Open,2021,11(5):e043605.
[11] YIN P,BRAUER M,COHEN A J,et al.The effect of air pollution on deaths,disease burden,and life expectancy across China and its provinces,1990-2017:an analysis for the Global Burden of Disease Study 2017[J].Lancet Planet Health,2020,4(9):e386-e398.
[12] TREPAT X,CHEN Z,JACOBSON K.Cell migration[J].Compr Physiol,2012,2(4):2369-2392.
[13] YEUNG K T,YANG J.Epithelial-mesenchymal transition in tumor metastasis[J].Mol Oncol,2017,11(1):28-39.
[14] BHOWMICK N A,MOSES H L.Tumor-stroma interactions[J].Curr Opin Genet Dev,2005,15(1):97-101.
[15] MITTAL V.Epithelial mesenchymal transition in tumor metastasis[J].Annu Rev Pathol,2018,13:395-412.
[16] SAHAI E.Mechanisms of cancer cell invasion[J].Curr Opin Genet Dev,2005,15(1):87-96.
[17] TASHIREVA L A,SAVELIEVA O E,GRIGORYEVA E S,et al.Heterogeneous manifestations of epithelial-mesenchymal plasticity of circulating tumor cells in breast cancer patients[J].Int J Mol Sci,2021,22(5):2504.
[18] JEONG S C,CHO Y,SONG M K,et al.Epidermal growth factor receptor (EGFR)-MAPK-nuclear factor(NF)-κB-IL8:a possible mechanism of particulate matter(PM) 2.5-induced lung toxicity[J].Environ Toxicol,2017,32(5):1628-1636.
[19] ZHENG L,LIU S,ZHUANG G,et al.Signal transductions of BEAS-2B cells in response to carcinogenic PM2.5 exposure based on a microfluidic system[J].Anal Chem,2017,89(10):5413-5421.
[20] LUO F,GUO H,YU H,et al.PM2.5 organic extract mediates inflammation through the ERbeta pathway to contribute to lung carcinogenesis in vitro and vivo[J].Chemosphere,2021,263:127867.
[21] HAN X,ZHUANG Y.PM2.5 induces autophagy-mediated cell apoptosis via PI3K/AKT/mTOR signaling pathway in mice bronchial epithelium cells[J].Exp Ther Med,2021,21(1):1.

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