MicroRNA-641 Inhibits Endometrial Cancer Progression via Targeting AP1G1.

ABSTRACT

MicroRNA-641 (miR-641) was significantly decreased in various cancers, but its roles in endometrial cancer (EC) remain unclear. We explored the influences of miR-641 on the EC cells. In our study, the miR-641 expression was reduced in EC cells. Overexpression of miR-641 inhibited viability and proliferation of HEC-1A and HECCL-1 cells by CCK-8 and colony formation assays. Additionally, flow cytometry revealed that overexpression of miR-641 could remarkably promote apoptosis and arrest the cell cycle at the G1 phase of HEC-1A and HECCL-1 cells. Besides, forced expression of miR-641 suppressed the migration and invasion of HEC-1A and HECCL-1 cells as evidenced by wound healing and transwell assay. Moreover, AP1G1 was confirmed as a target gene of miR-641 by StarBase prediction and DLR assay and their expressions were negatively correlated. Overexpression of AP1G1 neutralized the roles of miR-641 mimic on the viability, proliferation, apoptosis, and migration of HEC-1A and HECCL-1 cells. Our findings illustrated that miR-641 was reduced in the EC cells and AP1G1 antagonized the miR-641 mimic-induced inhibition of the EC progression in vitro. Therefore, miR-641 may emerge as an effective molecule for EC treatment.