OBJECTIVE: This study aimed to find out the regulatory mechanism of miR-194-5p targeting STAT1/mTOR signaling pathway on the biological characteristics of endometrial epithelium cells from mice with endometriosis (EMs). METHODS: Mouse model of EMs was constructed to observe the histopathological changes of endometrium via HE staining. The targeting relationship between miR-194-5p and STAT1 was verified by bioinformatics website as well as dual-luciferase reporter assay. The expressions of miR-194-5p and STAT1 in the cells were detected by qRT-PCR, then, the proliferative activity, invasion ability, apoptosis and cycle of cells were determined after overexpression of miR-194-5p, or down-regulation of miR-194-5p and STAT1. RESULTS: In the ectopic endometrial epithelial cells, the expression of miR-194-5p was reduced, while the expression of STAT1 was significantly elevated. Overexpression of miR-194-5p or down-regulation of STAT1 significantly inhibited the proliferation and invasion and promoted apoptosis of ectopic endometrial cells. While down-regulation of miR-194-5p reversed the results, and inhibition of STAT1 partially reversed the effects partially. CONCLUSIONS: The miR-194-5p inhibits mTOR signaling pathway by inhibiting the expression of STAT1 gene, so as to inhibit the proliferation and invasion, as well as to promote the apoptosis of ectopic endometrial epithelial cells in mice with EMs. AJTR
OBJECTIVE: This study aimed to find out the regulatory mechanism of miR-194-5p targeting STAT1/mTOR signaling pathway on the biological characteristics of endometrial epithelium cells from mice with endometriosis (EMs). METHODS:Mouse model of EMs was constructed to observe the histopathological changes of endometrium via HE staining. The targeting relationship between miR-194-5p and STAT1 was verified by bioinformatics website as well as dual-luciferase reporter assay. The expressions of miR-194-5p and STAT1 in the cells were detected by qRT-PCR, then, the proliferative activity, invasion ability, apoptosis and cycle of cells were determined after overexpression of miR-194-5p, or down-regulation of miR-194-5p and STAT1. RESULTS: In the ectopic endometrial epithelial cells, the expression of miR-194-5p was reduced, while the expression of STAT1 was significantly elevated. Overexpression of miR-194-5p or down-regulation of STAT1 significantly inhibited the proliferation and invasion and promoted apoptosis of ectopic endometrial cells. While down-regulation of miR-194-5p reversed the results, and inhibition of STAT1 partially reversed the effects partially. CONCLUSIONS: The miR-194-5p inhibits mTOR signaling pathway by inhibiting the expression of STAT1 gene, so as to inhibit the proliferation and invasion, as well as to promote the apoptosis of ectopic endometrial epithelial cells in mice with EMs. AJTR