lncRNA LA16c­313D11.11 modulates the development of endometrial cancer by binding to and inhibiting microRNA­205­5p function and indirectly increasing PTEN activity.

The aim of the present study was to determine the competitive endogenous RNA (ceRNA) network associated with long­coding RNA (lncRNA) LA16c­313D11.11 in endometrial cancer (EC). Initially, the expression levels of LA16c­313D11.11 in 60 EC tissues, 20 atypical hyperplasia endometrium (EAH) tissues and 20 normal endometrium tissues was determined. MicroRNA (miRNA/miR)­205­5p mimics and LA16c­313D11.11 mimics were transfected into HEC­1A and Ishikawa cells. The expression levels of miR­205­5p, LA16c­313D11.11 and their target proteins were assessed using reverse transcription­quantitative PCR or western blot analysis. Flow cytometry, Cell Counting kit­8 assays, Transwell migration assays and wound healing assays were performed to assess the effects of LA16c­313D11.11 and miR­205­5p on the migration and proliferation of tumor cells in vitro. The expression levels of LA16c­313D11.11 and phosphatase and tensin homolog deleted on chromosome ten (PTEN) in human EAH and EC tissues were significantly decreased, whereas the expression levels of miR­205­5p in EAH and EC tissues were significantly increased, compared with the normal endometrium tissues. The expression of LA16c­313D11.11 in human EC tissues negatively correlated with the expression of miR­205­5p. Additionally, the overexpression of LA16c­313D11.11 significantly reduced the invasion, migration and viability of HEC­1A and Ishikawa cells in vitro. LA16c­313D11.11 was shown to regulate the expression of PTEN, and the invasion, migration and viability of HEC­1A and Ishikawa cells, through its microRNA response element to compete for microRNA­205­5p. LA16c­313D11.11 was also shown to modulate the PI3K/AKT signaling pathway. Therefore, LA16c­313D11.11 acts as an effective ceRNA associated with a microRNA­205­5p­PTEN axis. LA16c­313D11.11 may inhibit the development and progression of EC by acting as a sponge of miR­205­5p, thus indirectly increasing the expression of PTEN.