@Article{096504016X14562725373798,
AUTHOR = {YaJie Cui, Kai’e She, Defu Tian, Peilian Zhang, Xiaoyan Xin},
TITLE = {miR-146a Inhibits Proliferation and Enhances Chemosensitivity in Epithelial  Ovarian Cancer via Reduction of SOD2},
JOURNAL = {Oncology Research},
VOLUME = {23},
YEAR = {2015},
NUMBER = {6},
PAGES = {275--282},
URL = {http://www.techscience.com/or/v23n6/57539},
ISSN = {1555-3906},
ABSTRACT = {Epithelial ovarian cancer (EOC) is the most lethal gynecological malignancy, accounting for 90% of all 
ovarian cancer. Dysregulation of miRNAs is associated with several types of EOC. In the current research, 
we aimed to study the role of abnormal expression of miR-146a in the development of EOC and to elucidate 
the possible molecular mechanisms. Compared with control samples, mRNA expression of miR-146a was 
significantly decreased in EOC tissues and cell lines. Overexpression of miR-146a prohibited cell proliferation, enhanced apoptosis, and increased sensitivity to chemotherapy drugs in EOC cells. In contrast, 
downregulation of miR-146a promoted cell proliferation, suppressed apoptosis, and decreased sensitivity 
to chemotherapy drugs in EOC cells. Overexpression of miR-146a increased the reactive oxygen species 
(ROS) level and decreased SOD2 mRNA and protein expression. Downregulation of miR-146a increased 
SOD2 mRNA and protein expression. Overexpression of SOD2 significantly inhibited miR-146a mimicsinduced suppression of cell proliferation and the increase of apoptosis and chemosensitivity. In conclusion, 
we identify miR-146a as a potential tumor suppressor in patients with EOC. miR-146a downregulates the 
expression of SOD2 and enhances ROS generation, leading to increased apoptosis, inhibition of proliferation, and enhanced sensitivity to chemotherapy. The data demonstrate that the miR-146a/SOD2/ROS pathway may serve as a novel therapeutic target and prognostic marker in patients with EOC.},
DOI = {10.3727/096504016X14562725373798}
}