Research Papers:
MicroRNA-16-5p overexpression suppresses proliferation and invasion as well as triggers apoptosis by targeting VEGFA expression in breast carcinoma
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Abstract
Yunhui Qu1,2,*, Hongtao Liu3,*, Xinquan Lv1, Yuqiong Liu1, Xiaojuan Wang1, Min Zhang1, Xiaqing Zhang3, Yuenan Li3, Qianqian Lou3, Shenglei Li1 and Huixiang Li1
1Department of Pathology, School of Basic Medical Sciences, Zhengzhou University and The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450001, Henan, P.R. China
2Clinical Laboratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450001, Henan, P.R. China
3Laboratory for Cell Biology, College of Life Sciences of Zhengzhou University, Zhengzhou, 450001, Henan, P.R. China
*These authors contributed equally to this work
Correspondence to:
Huixiang Li, email: [email protected]
Keywords: microRNA-16-5p, breast carcinoma, HIF-α, VEGFA, tumor growth
Received: March 03, 2017 Accepted: August 07, 2017 Published: August 23, 2017
ABSTRACT
MicroRNAs (miRNAs), a class of small noncoding RNA molecules, can manipulate the expressions of endogenous tumor-related genes, and are implicated in the development and progression of a wide type of tumors. In this study, the investigation from real-time quantitative PCR revealed that miRNA-16-5p was downregulated in breast carcinoma tissues and cells, coupled with the elevations of HIF-α and VEGFA protein expressions, compared with normal tissues. Lentiviral armed with miR-16-5p markedly increased the miR-16-5p levels in MCF-7 and MDA-MB-231 cells, compared to blank and NC groups, and miR-16-5p overexpression significantly inhibited the proliferation and colony formation in MCF-7 and MDA-MB-231 cells. Besides, miR-16-5p upregulation markedly induced apoptosis and reduced invasion ability in MCF-7 and MDA-MB-231 cells. Notably, VEGFA was direct target of miR-16-5p. Stepwise investigation from in vitro and in vivo experiments demonstrated that miR-16-5p overexpression suppressed tumor growth and reduced HIF-α and VEGFA expressions in breast carcinoma cells and nude mice tumor tissues. These findings provide novel insights into molecular mechanism involved in the roles of miR-16-5p in tumor development and progression of breast carcinoma, and thus manipulation of miR-16-5p may be a novel potential therapeutic target for future therapies of the patients with breast carcinoma.
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