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

Zhou,Fang; Li,Suli; Jia,Wenliang; Lv,Gang; Song,Chonglin; Kang,Chunsheng; Zhang,Qingyu

doi:10.3892/mmr.2015.3655

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

Authors:
- Fang Zhou
- Suli Li
- Wenliang Jia
- Gang Lv
- Chonglin Song
- Chunsheng Kang
- Qingyu Zhang
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Affiliations: Department of Gastroenterology, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China, State Key Laboratory of Internal Combustion Engine Fuel Science of Tianjin University, Tianjin 300072, P.R. China, Department of Neurosurgery, Tianjin Medical University General Hospital and Laboratory of Neuro-Oncology, Tianjin Neurological Institute, Tianjin 300052, P.R. China
Published online on: April 22, 2015 https://doi.org/10.3892/mmr.2015.3655
Pages: 2329-2335

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Abstract

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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