miR‑30c may serve a role in endometriosis by targeting plasminogen activator inhibitor‑1

Chen,Xiaoli; Jiang,Yan; Pan,Dianling

doi:10.3892/etm.2017.5145

miR‑30c may serve a role in endometriosis by targeting plasminogen activator inhibitor‑1

Authors:
- Xiaoli Chen
- Yan Jiang
- Dianling Pan
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Affiliations: 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, Department of Gynecology and Obstetrics, Jinan Maternity and Child Care Hospital, Jinan, Shandong 250000, P.R. China
Published online on: September 20, 2017 https://doi.org/10.3892/etm.2017.5145
Pages: 4846-4852
Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

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.

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