@Article{096504017X14974343584989,
AUTHOR = {Yanli Wang, Jia Li, Chunling Xu, Xiaomeng Zhang},
TITLE = {MicroRNA-139-5p Inhibits Cell Proliferation and Invasion by Targeting  RHO-Associated Coiled-Coil-Containing Protein Kinase 2 in Ovarian Cancer},
JOURNAL = {Oncology Research},
VOLUME = {26},
YEAR = {2018},
NUMBER = {3},
PAGES = {411--420},
URL = {http://www.techscience.com/or/v26n3/56653},
ISSN = {1555-3906},
ABSTRACT = {Increasing evidence indicates that the dysregulation of microRNAs is associated with the development and progression of various cancers. MicroRNA-139-5p (miR-139-5p) has been reported to have a tumor suppressive 
role in many types of cancers. The role of miR-139-5p in ovarian cancer (OC) is poorly understood. The purpose 
of the present study was to explore the expression of miR-139-5p and its function in OC. The results showed 
that miR-139-5p expression was markedly downregulated in OC tissues and cell lines. In addition, underexpression of miR-139-5p was significantly associated with FIGO stage, lymph mode metastasis, and poor 
overall survival of OC patients. Functional analyses indicated that overexpression of miR-139-5p significantly 
inhibited proliferation, colony formation, migration, and invasion of OC cells. Rho-associated coiled-coilcontaining protein kinase 2 (ROCK2) was identified as a direct target of miR-139-5p using luciferase reporter 
assays, qualitative real-time reverse transcriptase PCR (qRT-PCR), and Western blot. In addition, ROCK2 
expression was upregulated and was inversely correlated with miR-139-5p levels in OC tissues. Rescue experiments showed that overexpression of ROCK2 effectively reversed the inhibitory effect of OC cells induced by 
miR-139-5p. Most interestingly, in vivo studies indicated that miR-139-5p markedly suppressed the growth of 
tumors by repressing ROCK2 expression in nude mice. Taken together, these findings demonstrated that miR-
139-5p plays an important tumor suppressor role in OC by directly binding to ROCK2, providing a novel target 
for the molecular treatment of OC.},
DOI = {10.3727/096504017X14974343584989}
}