MiR-424-5p regulates proliferation and apoptosis by targeting FGFR1 in endometriosis cells

Objective: Endometriosis is a chronic disease that influences approximately 5-15% of women of reproductive age. Some studies have confirmed that numerous microRNAs (miRNAs) are unconventionally expressed in the ectopic endometrium. However, the accurate pathological mechanism of the effect of miRNAs on endometriosis is not completely clear. The aim of this study was to investigate the functional role of miR-424-5p in endometriosis. Methods: The levels of the miR-424-5p were detected by qRT-PCR. The protein levels of fibroblast growth factor receptor1 (FGFR1) and signal transducer and activator of transcription-3 (STAT3) were measured by western blot. Online software and luciferase reporter assay system were used to predict and verify the targets of miR-425-5p. Cell proliferation and apoptosis were examined in vitro by MTT and apoptosis assay. Results: The expression level of miR-424-5p was significantly downregulated, and the level of FGFR1 was significantly upregulated in the tissues from patients with endometriosis compared with normal endometrium. MiR-424-5p directly targeted FGFR1 and effectively inhibited FGFR1 expression in endometriosis cell line CRL-7566. In addition, miR-424-5p significantly suppressed proliferation and promoted apoptosis of CRL-7566 cells, whereas FGFR1 overexpression reversed the effect of miR-424-5p on CRL-7566 cells. Moreover, miR-424-5p reduced pSTAT3 expression, while FGFR1 overexpression attenuated the inhibitory effect of miR-424-5p on pSTAT3 expression in CRL-7566 cells. Conclusion: miR424-5p is down-regulated in the ectopic endometrium and regulates endometriosis cell proliferation and apoptosis through STAT3 signaling by targeting FGFR1.