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Effects of diesel exhaust particles on microRNA-21 in human bronchial epithelial cells and potential carcinogenic mechanisms

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Air pollution plays a role in cancer risk, particularly in lung cancer, which is the leading cause of cancerrelated 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 miR21 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 shortterm exposure to a high DEP concentration did not cause evident cell carcinogenesis in HBE cells.
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Document Type: Research Article

Affiliations: 1: Department of Gastroenterology, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China 2: State Key Laboratory of Internal Combustion Engine Fuel Science of Tianjin University, Tianjin 300072, P.R. China 3: Department of Neurosurgery, Tianjin Medical University General Hospital and Laboratory of Neuro-Oncology, Tianjin Neurological Institute, Tianjin 300052, P.R. China

Publication date: August 1, 2015

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  • Molecular Medicine Reports is a monthly, peer-reviewed journal available in print and online, that includes studies devoted to molecular medicine, underscoring aspects including pharmacology, pathology, genetics, neurosciences, infectious diseases, molecular cardiology and molecular surgery. In vitro and in vivo studies of experimental model systems pertaining to the mechanisms of a variety of diseases offer researchers the necessary tools and knowledge with which to aid the diagnosis and treatment of human diseases.
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