[1] |
Zhou M, He G, Fan M, et al. Smog episodes, fine particulate pollution and mortality in China. Environ Res, 2015; 136, 396−404. doi: 10.1016/j.envres.2014.09.038 |
[2] |
Song C, He J, Wu L, et al. Health burden attributable to ambient PM2.5 in China. Environ Pollut, 2017; 233, 575−86. doi: 10.1016/j.envpol.2017.01.060 |
[3] |
Zhan D, Kwan MP, Zhang W, et al. Spatiotemporal variations and driving factors of air pollution in China. Int J Environ Res Public Health, 2017; 14, 1538. doi: 10.3390/ijerph14121538 |
[4] |
Han L, W Zhou, W Li, et al. City as a major source area of fine particulate (PM2.5) in China. Environ Pollut, 2015; 206, 183−7. doi: 10.1016/j.envpol.2015.06.038 |
[5] |
Kisseleva T, Bhattacharya S, Braunstein J, et al. Signaling through the JAK/STAT pathway, recent advances and future challenges. Gene, 2002; 285, 1−24. doi: 10.1016/S0378-1119(02)00398-0 |
[6] |
Wu Y, Tian Y, Wang M, et al. Short-term exposure to air pollution and its interaction effects with two ABO SNPs on blood lipid levels in northern China: a family-based study. Chemosphere, 2020; 249, 126120. doi: 10.1016/j.chemosphere.2020.126120 |
[7] |
Liu Q, Baumgartner J, Schauer J. Source apportionment of fine-particle, water-soluble organic nitrogen and its association with the inflammatory potential of lung epithelial cells. Environ Sci Technol, Environ Sci Technol, 2019; 53, 9845−54. |
[8] |
Liu Q, Baumgartner J, Zhang Y, et al. Oxidative potential and inflammatory impacts of source apportioned ambient air pollution in Beijing. Environ Sci Technol, 2014; 48, 12920−9. doi: 10.1021/es5029876 |
[9] |
Li T, Hu R, Chen Z, et al. Fine particulate matter (PM2.5): the culprit for chronic lung diseases in China. Chronic Dis Transl Med, 2018; 4, 176−86. |
[10] |
Ning J, Li P, Zhang B, et al. miRNAs deregulation in serum of mice is associated with lung cancer related pathway deregulation induced by PM2.5. Environ Pollut, 2019; 254, 112875. doi: 10.1016/j.envpol.2019.07.043 |
[11] |
Gogna P, Narain TA, O'Sullivan DE, et al. Estimates of the current and future burden of lung cancer attributable to PM2.5 in Canada. Prev Med, 2019; 122, 91−9. doi: 10.1016/j.ypmed.2019.03.010 |
[12] |
Li R, Yang L, Jiang N, et al. Activated macrophages are crucial during acute PM2.5 exposure-induced angiogenesis in lung cancer. Oncol Lett, 2020; 19, 725−34. |
[13] |
Senecal A, Munsky B, Proux F, et al. Transcription factors modulate c-fos transcriptional bursts. Cell Rep, 2014; 8, 75−83. doi: 10.1016/j.celrep.2014.05.053 |
[14] |
Gutiérrez A, Sambuco L, Álvarez L, et al. Expression of estrogen receptor alpha variants and c-Fos in rat mammary gland and tumors. J Steroid Biochem Mol Biol, 2020; 199, 105594. doi: 10.1016/j.jsbmb.2020.105594 |
[15] |
Li X, W Wang, J Chen, et al. Recent progress in mass spectrometry proteomics for biomedical research. Sci China Life Sci, 2017; 60, 1093−113. doi: 10.1007/s11427-017-9175-2 |
[16] |
Yuan Q, Chen Y, Li X, et al. Ambient fine particulate matter (PM2.5) induces oxidative stress and pro-inflammatory response via up-regulating the expression of CYP1A1/1B1 in human bronchial epithelial cells in vitro. Mutat Res Genet Toxicol Environ Mutagen, 2019; 839, 40−8. doi: 10.1016/j.mrgentox.2018.12.005 |
[17] |
Ren X, Tang Y, Sun J, et al. Flavone protects HBE cells from DNA double-strand breaks caused by PM2.5. Hum Cell, 2018; 31, 116−26. doi: 10.1007/s13577-017-0193-7 |
[18] |
Liu W, Xu Y, Liu W, et al. Oxidative potential of ambient PM2.5 in the coastal cities of the Bohai Sea, northern China: seasonal variation and source apportionment. Environ Pollut, 2018; 236, 514−28. |
[19] |
Liu Q, Lu Z, Xiong Y, et al. Oxidative potential of ambient PM2.5 in Wuhan and its comparisons with eight areas of China. Sci Total Environ, 2020; 701, 134844. |
[20] |
Ross RA, Walton JD, Han D, et al. A distinct gene expression signature characterizes human neuroblastoma cancer stem cells. Stem Cell Res, 2015; 15, 419−26. doi: 10.1016/j.scr.2015.08.008 |
[21] |
Chouhan S, Singh S, Athavale D, et al. Glucose induced activation of canonical Wnt signaling pathway in hepatocellular carcinoma is regulated by DKK4. Sci Rep, 2016; 6, 27558. doi: 10.1038/srep27558 |
[22] |
Kim YJ, Lee G, Han J, et al. UBE2C overexpression aggravates patient outcome by promoting estrogen-dependent/independent cell proliferation in early hormone receptor-positive and HER2-negative breast cancer. Front Oncol, 2019; 9, 1574. |
[23] |
Yu PF, Kang AR, Jing LJ, et al. Long non-coding RNA CACNA1G-AS1 promotes cell migration, invasion and epithelial-mesenchymal transition by HNRNPA2B1 in non-small cell lung cancer. Eur Rev Med Pharmacol Sci, 2018; 22, 993−1002. |
[24] |
Kaplan A, CiftciAG, Kutlu HM. The apoptotic and genomic studies on A549 cell line induced by silver nitrate. Tumour Biol, 2017; 39, 1010428317695033. |
[25] |
Zhang Y, Yuan Z, Jiang Y, et al. Inhibition of splicing factor 3b subunit 1 (SF3B1) reduced cell proliferation, induced apoptosis and resulted in cell cycle arrest by regulating homeobox A10 (HOXA10) splicing in AGS and MKN28 human gastric cancer cells. Med Sci Monit, 2020; 26, e919460. |
[26] |
Ning Q, Pang Y, Shao S, et al. MicroRNA-147b suppresses the proliferation and invasion of non-small-cell lung cancer cells through downregulation of Wnt/beta-catenin signalling via targeting of RPS15A. Clin Exp Pharmacol Physiol, 2020; 47, 449−58. |
[27] |
Zhao X, Shen L, Feng Y, et al. Decreased expression of RPS15A suppresses proliferation of lung cancer cells. Tumour Biol, 2015; 36, 6733−40. |
[28] |
Hsu CH, Hsu CW, Hsueh C, et al. Identification and characterization of potential biomarkers by quantitative tissue proteomics of primary lung adenocarcinoma. Mol Cell Proteomics, 2016; 15, 2396−410. doi: 10.1074/mcp.M115.057026 |
[29] |
Zhang X, Wang W, Wang H, et al. Identification of ribosomal protein S25 (RPS25)-MDM2-p53 regulatory feedback loop. Oncogene, 2013; 32, 2782−91. doi: 10.1038/onc.2012.289 |
[30] |
Chen L, Wang H. Nicotine promotes human papillomavirus (HPV)-immortalized cervical epithelial cells (H8) proliferation by activating RPS27a-Mdm2-P53 pathway in vitro. Toxicol Sci, 2019; 167, 408−18. |