Lncrna La16c-313d11.11 Modulates The Development Of Endometrial Cancer By Binding To And Inhibiting Microrna-205-5p Function And Indirectly Increasing Pten Activity

The aim of the present study was to determine the competitive endogenous RNA (ceRNA) network associated with long-coding RNA (lncRNA) LA16c-313D11.11 in endometrial cancer (EC). Initially, the expression levels of LA16c-313D11.11 in 60 EC tissues, 20 atypical hyperplasia endometrium (EAH) tissues and 20 normal endometrium tissues was determined. MicroRNA (miRNA/miR)-205-5p mimics and LA16c-313D11.11 mimics were transfected into HEC-1A and Ishikawa cells. The expression levels of miR-205-5p, LA16c-313D11.11 and their target proteins were assessed using reverse transcription-quantitative PCR or western blot analysis. Flow cytometry, Cell Counting kit-8 assays, Transwell migration assays and wound healing assays were performed to assess the effects of LA16c-313D11.11 and miR-205-5p on the migration and proliferation of tumor cellsin vitro.The expression levels of LA16c-313D11.11 and phosphatase and tensin homolog deleted on chromosome ten (PTEN) in human EAH and EC tissues were significantly decreased, whereas the expression levels of miR-205-5p in EAH and EC tissues were significantly increased, compared with the normal endometrium tissues. The expression of LA16c-313D11.11 in human EC tissues negatively correlated with the expression of miR-205-5p. Additionally, the overexpression of LA16c-313D11.11 significantly reduced the invasion, migration and viability of HEC-1A and Ishikawa cellsin vitro.LA16c-313D11.11 was shown to regulate the expression of PTEN, and the invasion, migration and viability of HEC-1A and Ishikawa cells, through its microRNA response element to compete for microRNA-205-5p. LA16c-313D11.11 was also shown to modulate the PI3K/AKT signaling pathway. Therefore, LA16c-313D11.11 acts as an effective ceRNA associated with a microRNA-205-5p-PTEN axis. LA16c-313D11.11 may inhibit the development and progression of EC by acting as a sponge of miR-205-5p, thus indirectly increasing the expression of PTEN.