@Article{096504017X14953948675430,
AUTHOR = {Dan Jiao, Man Wu, Lei Ji, Feng Liu, Yingying Liu},
TITLE = {MicroRNA-186 Suppresses Cell Proliferation and Metastasis  Through Targeting Sentrin-Specific Protease 1 in Renal Cell Carcinoma},
JOURNAL = {Oncology Research},
VOLUME = {26},
YEAR = {2018},
NUMBER = {2},
PAGES = {249--259},
URL = {http://www.techscience.com/or/v26n2/56636},
ISSN = {1555-3906},
ABSTRACT = {Recent evidence suggests that dysregulation of microRNAs is associated with the development of multiple 
malignancies. miR-186 has been reported as a critical cancer regulator in several types of cancers. However, 
its functional significance and molecular mechanism underlying renal cell carcinoma (RCC) remain unknown. 
In this study, our results showed that miR-186 expression was dramatically downregulated in RCC tissues and 
cell lines compared to that in adjacent normal tissues and cell lines. Overexpression of miR-186 significantly 
inhibited cell growth, colony formation, and cell invasion; caused cell cycle arrest at the G<sub>0</sub>/G<sub>1</sub> phase; and 
induced cell apoptosis as detected by MTT, colony formation, Transwell assay, and flow cytometry assays in 
RCC cells. In addition, inhibition of miR-186 expression promoted RCC cell proliferation, invasion, and cell 
cycle progression and reduced apoptosis. Bioinformatics analysis and luciferase reporter assay confirmed that 
the 3'-UTR of sentrin-specific protease 1 (SENP1) was a direct target of miR-186. A remarkably reverse correlation was observed between miR-186 and SENP1 mRNA in RCC tissues. Furthermore, immunohistochemical 
staining revealed that SENP1 was positively expressed in RCC specimens. Restoration of SENP1 expression 
could partially abrogate the inhibitory effect of miR-186 overexpression on RCC cell proliferation through activating NF-kB signaling and its downstream proteins. These data demonstrated that miR-186 acted as a novel 
tumor suppressor and potential therapeutic biomarker in the progression of RCC by directly targeting SENP1.},
DOI = {10.3727/096504017X14953948675430}
}