MicroRNA-425 promotes the development of lung adenocarcinoma via targeting A disintegrin and metalloproteinases 9 (ADAM9)
Authors Liu R, Wang F, Guo Y, Yang J, Chen S, Gao X, Wang X
Received 26 December 2017
Accepted for publication 4 May 2018
Published 16 July 2018 Volume 2018:11 Pages 4065—4073
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Andrew Yee
Peer reviewer comments 3
Editor who approved publication: Professor Jianmin Xu
Ruibao Liu, Fang Wang, Yanchun Guo, Jianmei Yang, Shaoping Chen, Xin Gao, Xunguo Wang
Department of Oncology, Dongying People’s Hospital, Dongying, Shandong 257091, People’s Republic of China
Purpose: We aimed to investigate the roles of microRNA-425 (miR-425) in lung adenocarcinoma, as well as its possible regulatory mechanism.
Materials and methods: The miR-425 expression in lung adenocarcinoma tissues and cells was determined. The regulatory relationship between miR-425 and IL-6/STAT3 signaling was investigated. In addition, miR-425 was downexpressed in H1299 cells, and its effects on cell proliferation and apoptosis were determined. Furthermore, the target relationship between miR-425 and A disintegrin and metalloproteinases 9 (ADAM9) in lung adenocarcinoma cells was explored.
Results: The miR-425 was significantly downregulated in lung adenocarcinoma tissues and cells and was markedly inhibited by IL-6/STAT3 signaling. In addition, miR-425 expression was successfully overexpressed by transfection with pre-miR-425. Overexpression of miR-425 decreased the proliferation and colony formation of H1299 cells and promoted cell apoptosis markedly. Moreover, ADAM9 was revealed as a target of miR-425, and ADAM9 expression was negatively regulated by miR-425.
Conclusion: Our findings indicate that downregulation of miR-425 caused by IL-6/STAT3 signaling leads to loss of ADAM9 targeting, results in enhanced ADAM9 expression, and contributes to the development of lung adenocarcinoma. Thus, increasing miR-425 may be a promising therapeutic strategy for this disease.
Keywords: lung adenocarcinoma, microRNA-425, IL-6/STAT3 signaling, proliferation, apoptosis, A disintegrin and metalloproteinases 9
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