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

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

doi:10.3892/mmr.2015.3655

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

Mol Med Rep. 2015 Aug;12(2):2329-35. doi: 10.3892/mmr.2015.3655. Epub 2015 Apr 22.

Authors

Fang Zhou¹, Suli Li¹, Wenliang Jia¹, Gang Lv², Chonglin Song², Chunsheng Kang³, Qingyu Zhang¹

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.

PMID: 25901472
DOI: 10.3892/mmr.2015.3655

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.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Apoptosis / drug effects
Bronchi / drug effects
Bronchi / metabolism
Bronchi / pathology
Carcinogens / toxicity*
Cell Cycle / drug effects
Cell Line
Cell Line, Tumor
Cell Movement / drug effects
Collagen / chemistry
Drug Combinations
Epithelial Cells / drug effects*
Epithelial Cells / metabolism
Epithelial Cells / pathology
Gene Expression Regulation
Humans
Laminin / chemistry
MicroRNAs / agonists*
MicroRNAs / genetics
MicroRNAs / metabolism
PTEN Phosphohydrolase / genetics
PTEN Phosphohydrolase / metabolism
Particulate Matter / toxicity*
Phosphatidylinositol 3-Kinases / genetics
Phosphatidylinositol 3-Kinases / metabolism
Proteoglycans / chemistry
Proto-Oncogene Proteins c-akt / genetics
Proto-Oncogene Proteins c-akt / metabolism
Signal Transduction / drug effects
Vehicle Emissions / toxicity*

Substances

Carcinogens
Drug Combinations
Laminin
MIRN21 microRNA, human
MicroRNAs
Particulate Matter
Proteoglycans
Vehicle Emissions
matrigel
Collagen
Phosphatidylinositol 3-Kinases
Proto-Oncogene Proteins c-akt
PTEN Phosphohydrolase
PTEN protein, human