miR-200c suppresses endometriosis by targeting MALAT1 in vitro and in vivo

作者：Zongwen Liang, Yijie Chen, Yuan Zhao, Chaoyi Xu, Anqi Zhang, Qiong Zhang, Danhan Wang, Jing He, Wenfeng Hua, Ping Duan · 发表于：Stem Cell Research & Therapy · 年份：2017 · DOI：10.1186/s13287-017-0706-z · 被引用次数：114 · 研究领域：Endometriosis Research and Treatment、Endometrial and Cervical Cancer Treatments、Reproductive System and Pregnancy

BACKGROUND: Endometriosis is a common, benign, and estrogen-dependent disease characterized by pelvic pain and infertility. To date, the pathogenesis of endometriosis remains unclear. Recent studies have demonstrated that noncoding RNAs, including microRNAs and long noncoding RNAs, play important roles in the development of endometriosis. METHODS: Expression profiling of miRNAs in endometrial tissue was characterized using microarrays. The most differentially expressed miRNAs were confirmed using quantitative reverse transcriptase-polymerase chain reaction analysis in additional ectopic endometrial (n = 27) and normal endometrial (n = 12) tissues. For in-vitro functional studies, 5-ethynyl-2'-deoxyuridine incorporation assay, Transwell assay, and dual-luciferase reporter assay were used to measure the proliferation, migration, and luciferase activity of miR-200c and the predicted targets of miR-200c in primary endometrial stromal cells (HESCs) derived from human endometrial biopsies, respectively. For in-vivo therapeutic interventions, polymeric nanoparticles of polyethylenimine-polyethylene glycol-arginine-glycine-aspartic acid were used for delivery of miR-200c mimic and inhibitor to determine the therapeutic effect of miR-200c in a rat model of endometriosis. RESULTS: Exogenous overexpression of miR-200c inhibited the proliferation and migration of HESCs, which were mainly regulated by metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). In contrast, inhibition...