Abstract
The focal point of this research was the functional role of RP11-395G23.3 in endometrial cancer (EC). The expression of RP11-395G23.3, microRNA (miRNA)-205-5p, and their target proteins were detected by quantitative real-time polymerase chain reaction and western-blot analyses. Flow cytometry and proliferation, Transwell, and wound healing assays were used to detect the effects of RP11-395G23.3 and miRNA-205-5p on tumor cell migration and proliferation in vitro. RP11-395G23.3 expression was negatively related to miRNA-205-5p, but positively related to phosphatase and tensin homolog (PTEN) expression in human EC tissues. We discovered that low RP11-395G23.3 expression was significantly related to advanced histological grade and lymphovascular space invasion in EC patients. In addition, overexpression of RP11-395G23.3 significantly inhibited the proliferation, invasion, migration, and induced apoptosis of Ishikawa and HEC-1A cells in vitro. Our results also showed that RP11-395G23.3 could directly bind to miRNA-205-5p through its miRNA response elements and eliminate the inhibitory effect of targeting gene PTEN, thus leading to the signaling pathway of phosphatidylinositol-3-kinase/AKT inactivation. We demonstrated for the first time that RP11-395G23.3 may inhibit the development and pathogenesis of EC by acting as a sponge for miRNA-205-5p and increasing PTEN expression. RP11-395G23.3 may be a target for the diagnosis and treatment of EC.