miR-155-5p Inhibits Decidualization in Endometrial Stromal Cells by Downregulating FOXO3a Expression

Abstract

Objective: FOXO3a has been reported to be involved in regulating decidual formation. This research aimed to probe into the role and mechanism of miR-155-5p/FOXO3a in the decidualization of endometrial stromal cells. Methods: Human endometrial stromal cells (hESCs) were cultured and decidualization induced in vitro. An immunofluorescence assay was utilized to monitor cell morphology. Quantitative RT-PCR (qRT-PCR) was applied to monitor the expression of microRNA-155-5p (miR-155-5p) in the decidualization model in vitro, ELISA was utilized to detect the levels of prolactin and Insulin-like growth factor binding protein 1 (IGFBP1). The levels of prolactin, IGFBP1, decorin (DCN), and Forkhead box O3 (FOXO3a) were detected by western blot. Dual-luciferase reporter gene assay was applied to detect the binding between miR-155-5p and FOXO3a. Results: The expression of miR-155-5p was downregulated in the process of decidualization. Herein, overexpression of miR-155-5p attenuated decidualization of hESCs in vitro. Compared with normal decidualized cells, the decidualization markers (prolactin, IGFBP1, and DCN) in miR-155-5p mimic-transfected cells were also inhibited. Furthermore, bioinformatics analysis and luciferase reporter analysis proved that FOXO3a was the direct target of miR-155-5p. The rescue experiment confirmed that FOXO3a could partially reverse the inhibition of miR-155-5p on decidualization. Conclusions: This study confirmed the regulatory function of miR-155-5p in the inhibition of FOXO3a-mediated decidualization. This may provide some understanding for the treatment of planting-related diseases and infertility.