Abstract
MicroRNA (miRNA/miR)‑21‑5p has been proposed as an oncogenic miRNA in human tumors; however, the exact role of miR‑21‑5p has not been fully determined in endometrial cancer. SRY‑box 17 (SOX17) is associated with endometrial cancer development and progression; however, the regulatory mechanisms underlying SOX17 expression in endometrial cancer remain unclear. In the present study, tumor samples were collected from 160 postmenopausal women with endometrial cancer. All tumor samples were examined for miR‑21‑5p expression by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). The results demonstrated that miR‑21‑5p expression was associated with shorter overall survival. In addition, overexpression of miR‑21‑5p promoted epithelial to mesenchymal transition (EMT), whereas silencing miR‑21‑5p reversed EMT in endometrial cancer cell lines. Using RT‑qPCR and western blotting, it was revealed that overexpressing miR‑21‑5p significantly inhibited SOX17 protein expression in endometrial cancer cell lines. Furthermore, as determined by luciferase reporter assay, ectopic expression of miR‑21‑5p inhibited the activity of the SOX17 mRNA 3'‑untranslated region (3'UTR), whereas silencing miR‑21‑5p promoted the activity of the SOX17 mRNA 3'UTR in endometrial cancer cell lines. Overexpression of SOX17 promoted mesenchymal to epithelial transition, whereas silencing SOX17 induced EMT in endometrial cancer cell lines. In addition, tumor SOX17 expression was associated with better overall survival. Therefore, it may be concluded that miR‑21‑5p promotes EMT by targeting SOX17 in human endometrial cancer.