Background: Endometrial cancer (EC) is the fourth most common malignancy among women. Epithelial to mesenchymal transition (EMT) and invasion have been identified as central cellular processes in tumor progression and malignant transformation. The function and molecular basis of microRNA-20a-5p (miR-20a-5p) in the development of EC are poorly defined.
Methods: RT-qPCR assay was used to detect the levels of miR-20a-5p and signal transducer and activator of transcription 3 (STAT3) mRNA. Western blot assay was conducted to determine protein expression of STAT3, N-cadherin, Vimentin and E-cadherin. Cell invasive capacity was examined by transwell invasion assay. Bioinformatics analysis, luciferase reporter assay and RIP assay were performed to investigate the interaction between miR-20a-5p and STAT3 3'UTR.
Results: miR-20a-5p expression was strikingly reduced in EC tissues and cells. Functional analysis revealed that miR-20a-5p overexpression inhibited EMT and invasion of EC cells. Further exploration showed that miR-20a-5p inhibited STAT3 expression by direct interaction. Moreover, the knockdown of STAT3 suppressed EMT and invasion of EC cells. Additionally, the depletion of STAT3 weakened miR-20a-5p downregulation-induced cell EMT and invasion in EC.
Conclusion: miR-20a-5p inhibited EMT and invasion of EC cells by targeting STAT3, highlighting the vital roles of miR-20a-5p and STAT3 in the metastasis and malignant transformation of EC.
Keywords: STAT3; endometrial cancer; epithelial to mesenchymal transition; invasion; microRNA-20a-5p.
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