MiR-223-3p Inhibitor Represses Endometrial Stromal Cell Progression by Targeting FBXW7

Background: This study aims to reveal the regulatory networks involving miR-223-3p in endometriosis.Methods: The expression levels of miR-223-3p and FBXW7 and their correlations in ectopic, eutopic and normal endometrial tissues were determined by qRT-PCR and Pearson correlation test. We isolated and identified primary endometriosis ectopic endometrial stromal cells (ESCs) and normal endometrial cells. The prediction on downstream targets of miR-223-3p was per-formed by bioinformatic analysis. The association of miR-223-3p with its downstream gene FBXW7 was confirmed by adopting the dual-luciferase reporter experiment. After transfection, cell function experiments were undertaken to detect cell biological behaviors. Determining levels of miR-223-3p and FBXW7 in ESCs was conducted by utilising qRT-PCR and Western blot.Results: MiR-223-3p was highly expressed, whilst FBXW7 was less expressed in eutopic and ectopic endometria. The ectopic ESCs and normal human endometrial cells were negative for CK19, but positive for Vimentin. FBXW7 levels were conversely related with miR-223-3p levels in normal, eutopic and ectopic endometria. MiR-223-3p mimic facilitated biological behaviors of human ESCs, whereas the opposite effect was seen with miR-223-3p inhibitor. Moreover, miR-223-3p inhibitor alleviated cell biological behaviors of human ESCs via elevating FBXW7 expression. Conclusions: miR-223-3p inhibitor restrains ESC progression via elevating FBXW7 expression.

Automated summary

This study reveals the regulatory networks involving miR-223-3p in endometriosis and finds that miR-223-3p inhibitor restrains the progression of ESCs by elevating FBXW7 expression.