MicroRNA-199a/b-5p inhibits endometrial cancer cell metastasis and invasion by targeting FAM83B in the epithelial-to-mesenchymal transition signaling pathway

Our previous study demonstrated the role of family with sequence similarity 83, member B (FAM83B) in endometrial cancer tumorigenesis and metastasis. FAM83B is involved in epithelial-to-mesenchymal transition (EMT). However, the regulatory network of EMT, which promotes endometrial cancer cell metastasis, involving microRNAs (miRNAs/miRs) and FAM83B, has not been elucidated. To investigate the potential mechanism underlying miR-199a/b-5p in endometrial cancer, the effect of miR-199a/b-5p and its targeted FAM83B gene on the biological behaviour of endometrial cancer cells was assessed. The Gene Expression Omnibus dataset analysis results revealed that the expression levels of 150 miRNAs in non-cancerous endometrial tissues were upregulated compared with those in endometrial cancer tissues. TargetScan predicted that the nucleotides 672–679 of FAM83B 3′-untranslated region (UTR) were the target sites of miR-199a/b-5p. The differentially expressed miRNAs were enriched in several Kyoto Encyclopedia of Genes and Genomes pathways. Reverse transcription-quantitative PCR analysis revealed that the expression levels of miR-199a/b-5p in the endometrial non-cancerous cell lines were significantly upregulated compared with those in the six endometrial cancer cell lines. miR-199a/b-5p inhibited the EMT signaling pathway by regulating the expression levels of E-cadherin, N-cadherin, Snail, α-smooth muscle actin, vimentin and Twist. This suggested that miR-199a/b-5p inhibited endometrial cancer cell proliferation and migration through the inhibition of the EMT signaling pathway. Furthermore, the nucleotides 672–679 of the FAM83B 3′-UTR were demonstrated to be the binding site of miR-199a/b-5p. These results suggested that miR-199a/b-5p inhibited endometrial cancer cell proliferation and metastasis by targeting the 3′-UTR of FAM83B, which is involved in the EMT signaling pathway.