miRNA-223 expression in patient-derived eutopic and ectopic endometrial stromal cells and its effect on epithelial-to-mesenchymal transition in endometriosis

Abstract

Objective:

This 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.

Methods:

Endometrial 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.

Results:

There 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.

Conclusion:

miRNA-223 expression decreased in endometrial SCs from endometriosis patients, which may facilitate the differential regulation of EMT during endometriosis.

Clinical Trial registration number: SWYX2020-211.

Keywords:
miRNA-223; Endometriosis; SCs; Epithelial-to-mesenchymal transition; Migration; Proliferation; Apoptosis

HIGHLIGHTS

miRNA-223 was downregulated in endometrial stromal ells from endometriosis patients.

miRNA-223 upregulation repressed malignant behaviors of endometrial stromal cells.

miRNA-223 might serve as a potential therapeutic target for endometriosis.