MiR-203 inhibits cell proliferation, invasion, and migration of ovarian cancer through regulating RGS17

It has been reported that G-protein signaling 17 (RGS17) oncogene is involved in the occurrence and development of ovarian cancer (OC), but the regulatory mechanism of OC is still unclear. MicroRNA (miRNA) negatively regulates gene expression, and its maladjustment is related to tumorigenesis. We understand the role of miRNA in OC modulators induced by RGS17. To characterize the regulatory effect of miR-203 on RGS17, we used ovarian cancer cell lines SKOV3 and OVCAR3, and constructed miR-203 and RGS17 overexpression vectors. CCK8 kit was used to detect cell proliferation, while Transwell analysis was used to measure cell invasion and migration. RT-qPCR and Western blotting were used to analyze the expression of miR-203 and RGS17 in ovarian cancer. The interaction between miR-203 and RGS17 was detected by fluorescent enzyme reporter gene method. The expression of miR-203 was significantly decreased in tumor cells, while the expression of RGS17 mRNA was increased. Luciferase reporter gene assay showed that miR-203 down regulated RGS17 expression by directly integrating into RGS17 mRNA. Our results showed that miR-203 was down regulated during tumorigenesis and inhibited the proliferation and invasion of OC cells. MiR-203 inhibits the proliferation, invasion and migration of ovarian cancer cell lines SKOV3 and OVCAR3 by targeting RGS17. After RGS17 overexpression, the regulatory effect of miR-203 was inhibited.