MiR-153 inhibits migration and invasion of human non-small-cell lung cancer by targeting ADAM19.

Autor: Shan N; Department of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, PR China; Institute of Medical Sciences, Xiangya Hospital, Central South University, Changsha, Hunan 410008, PR China., Shen L; Department of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, PR China., Wang J; Institute of Medical Sciences, Xiangya Hospital, Central South University, Changsha, Hunan 410008, PR China., He D; Institute of Medical Sciences, Xiangya Hospital, Central South University, Changsha, Hunan 410008, PR China., Duan C; Department of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, PR China; Institute of Medical Sciences, Xiangya Hospital, Central South University, Changsha, Hunan 410008, PR China. Electronic address: duancjxy@163.com.
Jazyk: angličtina
Zdroj: Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2015 Jan 02; Vol. 456 (1), pp. 385-91. Date of Electronic Publication: 2014 Dec 02.
DOI: 10.1016/j.bbrc.2014.11.093
Abstrakt: MiR-153 was reported to be dysregulated in some human cancers. However, the function and mechanism of miR-153 in lung cancer cells remains unknown. In this study, we investigated the role of miR-153 in human non-small-cell lung cancer (NSCLC). Using qRT-PCR, we demonstrated that miR-153 was significantly decreased in clinical NSCLC tissues and cell lines, and downregulation of miR-153 was significantly correlated with lymph node status. We further found that ectopic expression of miR-153 significantly inhibited the proliferation and migration and invasion of NSCLC cells in vitro, suggesting that miR-153 may be a novel tumor suppressor in NSCLC. Further integrated analysis revealed that ADAM19 is as a direct and functional target of miR-153. Luciferase reporter assay demonstrated that miR-153 directly targeted 3'UTR of ADAM19, and correlation analysis revealed an inverse correlation between miR-153 and ADAM19 mRNA levels in clinical NSCLC tissues. Knockdown of ADAM19 inhibited migration and invasion of NSCLC cells which was similar with effects of overexpression of miR-153, while overexpression of ADAM19 attenuated the function of miR-153 in NSCLC cells. Taken together, our results highlight the significance of miR-153 and ADAM19 in the development and progression of NSCLC.
(Copyright © 2014 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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