Abstract: Objective To investigate the effect and mechanism of FAM83H-AS1 on epithelial-mesenchymal transition (EMT) and angiogenesis in endometrial cancer cells. Methods Human endometrial cancer Ishikawa cells were divided into four groups: Blank group, FAM83H-AS1 siRNA group (transfected with FAM83H-AS1 siRNA), miR-4684-5p mimics group (transfected with miR-4684-5p mimics), and FAM83H-AS1 siRNA + miR-4684-5p mimics group (co-transfected with FAM83H-AS1 siRNA and miR-4684-5p mimics). Cell invasion was detected by Transwell assay; tube formation was detected by Matrigel assay; the EMT marker proteins E-cadherin and Vimentin were detected by Western blot; the targeted relationship between FAM83H-AS1 and miR-4684-5p was detected by dual-luciferase reporter assay; and the expression levels of FAM83H-AS1 and miR-4684-5p were detected by qPCR. Results Compared with the Blank group, the expression of FAM83H-AS1 was decreased and the expression of miR-4684-5p was increased in FAM83H-AS1 siRNA group and the miR-4684-5p mimics group(P＜0.05). Compared with the FAM83H-AS1 siRNA group or the miR-4684-5p mimics group, the expression of FAM83H-AS1 was decreased and the expression of miR-4684-5p was increased in the FAM83H-AS1 siRNA + miR-4684-5p mimics group (P＜0.05), among which there was no statistically significant difference between the FAM83H-AS1 siRNA group and the miR-4684-5p mimics group. Compared with the blank group, the number of cell invasions, tube formations, and the protein level of Vimentin were all decreased, while E-cadherin was increased in the FAM83H-AS1 siRNA group and the miR-4684-5p mimics group (P＜0.05). Compared with the FAM83H-AS1 siRNA group or the miR-4684-5p mimics group, the number of cell invasions, tube formations, and the protein level of vimentin were all decreased, while E-cadherin was increased in the FAM83H-AS1 siRNA+miR-4684-5p mimics group (P＜0.05), among which there was no statistically significant difference between the FAM83H-AS1 siRNA group and the miR-4684-5p mimics group. The dual-luciferase reporter assay showed that after transfection with miR-4684-5p mimics, the activity in the FAM83H-AS1 3′UTR-WT group was significantly reduced (P＜0.05), whereas the effect on the FAM83H-AS1-3′UTR-MUT group was not significant. Conclusions In the endometrial cancer cell line Ishikawa, knockdown of FAM83H-AS1 or overexpression of miR-4684-5p inhibits epithelial-mesenchymal transition and angiogenesis, an effect mediated by the targeted regulation of miR-4684-5p.

Key words: FAM83H-AS1, miR-4684-5p, endometrial cancer, epithelial-mesenchymal transition (EMT), angiogenesis