期刊
MOLECULAR MEDICINE REPORTS
卷 12, 期 2, 页码 2329-2335出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2015.3655
关键词
diesel exhaust particles; normal human bronchial epithelial cells; lung adenocarcinoma cells; microRNA-21; antisense oligonucleotide of microRNA-21; morphology
资金
- State Key Laboratory of Internal Combustion Engine Fuel Science of Tianjin University [K2011-04]
Air pollution plays a role in cancer risk, particularly in lung cancer, which is the leading cause of cancer-related mortality worldwide. Diesel exhaust particles (DEPs), a component of diesel exhaust products, is a complex mixture of particle compounds that include a large number of known and suspected human carcinogens. Historically, lung cancer, which is associated with DEPs, has been the focus of attention as a health risk in human and animal studies. However, the mechanism by which DEPs cause lung cancer remains unclear. The present study reports that DEPs increased miR-21 expression and then activated the PTEN/PI3K/AKT pathway in human bronchial epithelial (HBE) cells, which may serve as an important carcinogenic mechanism. However, the data revealed that short-term exposure to a high DEP concentration did not cause evident cell carcinogenesis in HBE cells.
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