Chen Xiaoli, Jiang Yan, Pan Dianling
Department of Reproductive Medicine, Affiliated Hospital of Jining Medical University, Jining, Shandong 272000, P.R. China.
Department of Gynecology and Obstetrics, Tengzhou Maternity and Child Care Hospital, Tengzhou, Shandong 277500, P.R. China.
Exp Ther Med. 2017 Nov;14(5):4846-4852. doi: 10.3892/etm.2017.5145. Epub 2017 Sep 20.
The present study aimed to investigate the role of miR-30c in endometriosis (EMs) and the underlying mechanism. The expression of miR-30c and plasminogen activator inhibitor type 1 (PAI-1) mRNA in EMs tissues was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and the expression of PAI-1 protein was detected by western blot analysis. The proliferation, migration, invasion and adhesion of endometrial stromal cells (ESCs) in different groups transfected with miR-30c mimic or inhibitor were compared. It was demonstrated that miR-30c expression in ectopic and eutopic endometriosis tissues were significantly lower than in normal endometrial tissue. However, PAI-1 mRNA expression in ectopic and eutopic endometrial tissues was higher than in normal endometrial tissues. Furthermore, the expression of PAI-1 protein was higher in ectopic and eutopic endometrosis tissues than in normal tissues. RT-qPCR results indicated that miR-30c expression was significantly increased or decreased in ESCs following transfection of mimic or inhibitor of miR-30c, respectively. Overexpression of miR-30c repressed the expression of PAI-1 mRNA and protein, while inhibition of miR-30c upregulated the expression of PAI-1 in ESCs. In addition, the invasion, migration, proliferation and adhesion of ESCs was repressed following the overexpression of miR-30c, whereas they were promoted when miR-30c expression was downregulated. The results of the present study indicated that miR-30c serves an important role in the development and progression of EMs by regulating the expression of PAI-1.
本研究旨在探讨miR-30c在子宫内膜异位症（EMs）中的作用及其潜在机制。采用逆转录-定量聚合酶链反应（RT-qPCR）检测EMs组织中miR-30c和纤溶酶原激活物抑制剂1（PAI-1）mRNA的表达，并通过蛋白质印迹分析检测PAI-1蛋白的表达。比较转染miR-30c模拟物或抑制剂的不同组子宫内膜基质细胞（ESCs）的增殖、迁移、侵袭和黏附情况。结果表明，异位和在位子宫内膜异位症组织中miR-30c的表达明显低于正常子宫内膜组织。然而，异位和在位子宫内膜组织中PAI-1 mRNA的表达高于正常子宫内膜组织。此外，异位和在位子宫内膜异位症组织中PAI-1蛋白的表达高于正常组织。RT-qPCR结果表明，分别转染miR-30c模拟物或抑制剂后，ESCs中miR-30c的表达显著增加或降低。miR-30c的过表达抑制了PAI-1 mRNA和蛋白的表达，而抑制miR-30c则上调了ESCs中PAI-1的表达。此外，miR-30c过表达后ESCs的侵袭、迁移、增殖和黏附受到抑制，而当miR-30c表达下调时则受到促进。本研究结果表明，miR-30c通过调节PAI-1的表达在EMs的发生和发展中起重要作用。
