Abstract
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 cells in 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 cells in 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.