Open Access

ARTICLE

Overexpression of MicroRNA-27b Inhibits Proliferation, Migration, and Invasion via Suppression of MET Expression

Hui Zhou^*†, Yanglin Liu^†, Ling Xiao^‡, Zhengmao Hu^*, Kun Xia^*§

* The State Key Laboratory of Medical Genetics, School of Life Sciences, Central South University, Changsha, Hunan, P.R. China
† The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, P.R. China
‡ Department of Histology and Embryology, School of Basic Medical Sciences, Central South University, Changsha, Hunan, P.R. China
§ Key Laboratory of Medical Information Research, Central South University, Changsha, P.R. China

Oncology Research 2017, 25(1), 147-154. https://doi.org/10.3727/096504016X14732772150505

Abstract

MicroRNA-27b (miR-27b) was recently found to be significantly downregulated in different human cancers. However, evidence of the function of miR-27b in non-small cell lung cancer (NSCLC) remains limited. In this study, we aimed to investigate novel miR-27b-mediated targets or signaling pathways associated with the tumorigenesis and metastasis of NSCLC. Real-time (RT) PCR was performed to examine miR-27b expression in NSCLC specimens. MTT assay, wound-healing assay, and Transwell assay were used to determine cell proliferation, migration, and invasion. Our data indicated that the miR-27b levels were significantly decreased in NSCLC specimens and cell lines (SK-MES-1, H358, H460, A549, and H1229) when compared to matched normal adjacent tissues and normal human lung epithelial cell lines, respectively. Restoration of miR-27b significantly inhibited the proliferation, migration, and invasion of A549 cells. We then conducted in silico analysis and luciferase reporter gene assay and identified MET, a receptor tyrosine kinase, as a direct target of miR-27b in NSCLC cells. Moreover, overexpression of MET rescued the suppressive effect of miR-27b on the proliferation, migration, and invasion of A549 cells, suggesting that MET acts as a downstream effecter of miR-27b in NSCLC cells. In summary, our study identified a novel miR-27b/MET signaling pathway involved in the cell proliferation, migration, and invasion of NSCLC, and identification of miR-27b-mediated novel signaling pathways may help reveal the molecular mechanism underlying the development and malignant progression of this disease.

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