[No authors listed]
MicroRNA (miRNA/miR)â21â5p has been proposed as an oncogenic miRNA in human tumors; however, the exact role of miRâ21â5p has not been fully determined in endometrial cancer. SRYâbox 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 160Â postmenopausal women with endometrial cancer. All tumor samples were examined for miRâ21â5p expression by reverse transcriptionâquantitative polymerase chain reaction (RTâqPCR). The results demonstrated that miRâ21â5p expression was associated with shorter overall survival. In addition, overexpression of miRâ21â5p promoted epithelial to mesenchymal transition (EMT), whereas silencing miRâ21â5p reversed EMT in endometrial cancer cell lines. Using RTâqPCR and western blotting, it was revealed that overexpressing miRâ21â5p significantly inhibited SOX17 protein expression in endometrial cancer cell lines. Furthermore, as determined by luciferase reporter assay, ectopic expression of miRâ21â5p inhibited the activity of the SOX17 mRNA 3'âuntranslated region (3'UTR), whereas silencing miRâ21â5p 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 miRâ21â5p promotes EMT by targeting SOX17 in human endometrial cancer.
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