
@Article{096504016X14732772150505,
AUTHOR = {Hui Zhou, Yanglin Liu, Ling Xiao, Zhengmao Hu, Kun Xia},
TITLE = {Overexpression of MicroRNA-27b Inhibits Proliferation, Migration,  and Invasion via Suppression of MET Expression},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {1},
PAGES = {147--154},
URL = {http://www.techscience.com/or/v25n1/56792},
ISSN = {1555-3906},
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.},
DOI = {10.3727/096504016X14732772150505}
}



