Journal
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
Volume 40, Issue 2, Pages 541-548Publisher
ELSEVIER
DOI: 10.1016/j.etap.2015.08.009
Keywords
Radon; MicroRNA; Let-7; K-ras
Funding
- National Natural Science Foundation of China [81402626, 81172707, 81302382]
- Natural Science Fund for colleges and universities in Jiangsu Province [12KJB330005]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
- Graduate Innovation Project of Jiangsu province [CXZZ13_0841]
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Radon has long been recognized as a human carcinogen leading to lung cancer, but the underlying mechanisms remain obscure. Recent studies have shown that the let-7 microRNA and K-ras play an important role in the development of various cancers. However, the exact role between let-7 and K-ras in radon induced lung damage has not been explored so far. In the present study, wistar rats and human bronchial epithelial (HBE) cells were long-term exposed to radon, and then alterations in histological pathology of rat lung tissue, ROS, antioxidant enzymes activities and clonogenic formation in HBE cells, as well as changes in let-7 and K-ras expression were determined to observe the adverse effects induced by radon. The results showed that long-term exposure to radon produced severe lung damage in rats, significantly increased ROS production and clonogenic formation ratios and decreased SOD activities in HBE cells. In addition, an obvious down-regulation of let-7 and up-regulation of K-ras were also revealed both in mRNA and in protein level in lung tissue of rats and HBE cells exposed to radon. Furthermore, a significant down-regulation of K-ras was then confirmed in both let-7b-3p and let-7a-2-3p transfected HBE cells. Taken together, the present results propose an involvement of let-7 microRNA and K-ras in radon induced lung damage both in vivo and in vitro, which may thus be of potential value in early diagnosis and therapy of radon-induced lung tumorgenesis. (C) 2015 Elsevier B.V. All rights reserved.
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