• Yuan Xue, Xueyan Lin, Tingting Shi, and Yongjie Tian.
• Department of Obstetrics and Gynecology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Shandong, China.
• Clinics (Sao Paulo). 2022 Jan 1; 77: 100112100112.

ObjectiveThis study was designed to evaluate the expression of microRNA-223 (miRNA-223) in patient-derived eutopic and ectopic endometrial stromal cells (SCs). Given the fact that miRNA-223 was previously shown to be upregulated in these cells and that this upregulation has been linked to epithelial-to-mesenchymal transition (EMT) during endometriosis, this study aimed to further explore the expression of miRNA-223, its effect in endometriosis, and the mechanisms underlying its effects.MethodsEndometrial tissue was collected from 26 patients with endometriosis and 14 patients with hysteromyoma (control group). Primary endometrial SCs were isolated and cultured from several endometrial samples and miRNA-223 expression was evaluated using qRT-PCR. Cells were then transfected with a miRNA-223 overexpression lentiviral vector (sh-miR-223 cells) or an empty control (sh-NC cells) and then used to monitor the effects of miRNA-223 on the expression of several EMT-associated proteins, including N-cadherin, vimentin, and Slug, using western blot. Cellular migration, invasion, and proliferation were then evaluated using a wound healing, Transwell, and CCK-8 assay, respectively. Flow cytometry was used to detect apoptosis.ResultsThere was a significant decrease in the expression of miRNA-223 in both eutopic and ectopic endometrial SCs (p < 0.05) whereas upregulation of miRNA-223 inhibited the expression of EMT-related molecules and reduced cell migration, invasion, and proliferation. High levels of miRNA-223 also promoted apoptosis.ConclusionmiRNA-223 expression decreased in endometrial SCs from endometriosis patients, which may facilitate the differential regulation of EMT during endometriosis.Clinical Trial Registration NumberSWYX2020-211.Copyright © 2022 HCFMUSP. Published by Elsevier España, S.L.U. All rights reserved.

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