摘要
Abstract
Objective To investigate the effect and mechanism of FAM83H-AS1 on epithelial-mesenchymal transi-tion(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 in-creased 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 theFAM83H-AS1-3′UTR-MUTgroup was not significant.Conclusions In the endometrial cancer cell line Ishikawa,knockdown of FAM83H-AS1 or overexpression of miR-4684-5p inhib-its epithelial-mesenchymal transition and angiogenesis,an effect mediated by the targeted regulation of miR-4684-5p.关键词
子宫内膜癌/FAM83H-AS1/miR-4684-5p/上皮-间质转化/血管生成Key words
FAM83H-AS1/miR-4684-5p/endometrial cancer/epithelial-mesenchymal transition(EMT)/angiogenesis分类
医药卫生
