Conclusion
Higher expression of AFAP1-AS1 positively correlated with greater EMT in ectopic endometrium of patients with endometriosis. Knockdown of AFAP1-AS1 inhibited E2-induced activity of promoter site pGL3-P886 of transcription factor ZTB1, suggesting that AFAP1-AS1 knockdown inhibited growth of endometrial epithelial cells and that pathogenesis may be correlated with EMT.
Results
AFAP1-AS1 levels were much higher in ectopic endometrial tissues than that in eutopic tissues. Expression of ZEB1, E-cadherin, and keratin was obviously higher in eutopic tissues than those in ectopic tissues. In contrast, expression of vimentin and N-cadherin was significantly lower in eutopic tissue than those in ectopic tissues. After knockdown of AFAP1-AS1, the morphology of endometrial epithelial cells varied from spindle fiber shaped to polygon epithelioid and proliferation, migration, and invasion were each inhibited. The knockdown of AFAP1-AS1 significantly inhibited expression from promoter site pGL3-P886 of the EMT-related transcription factor ZEB1. The size of subcutaneous tumours in nude mice was significantly reduced after down-regulation of AFAP1-AS1 expression.