Long non‐coding RNA AFAP1‐AS1 promoting epithelial‐mesenchymal transition of endometriosis is correlated with transcription factor ZEB1

Dianchao Lin, Qiansheng Huang, Rongfeng Wu, Song‐Juan Dai, Songjuan Dai, Zhixiong Huang, Lulu Ren, Sijing Huang, Qionghua Chen
American journal of reproductive immunology (New York, N.Y. : 1989) · 2018 · vol. 81(1) , pp. e13074 · doi:10.1111/aji.13074 · PMID:30506548 · W2903069512
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Long non-coding RNA AFAP1-AS1 is highly expressed in ectopic endometrial tissues of endometriosis patients and promotes epithelial-mesenchymal transition, correlating with transcription factor ZEB1.

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Abstract

PROBLEM: The role of the long non-coding RNA (lncRNA) actin filament associated protein 1 antisense RNA1 (AFAP1-AS1) in the etiology of endometriosis is unknown. METHOD OF STUDY: Expression of epithelial-mesenchymal transition (EMT) markers was quantified using qRT-PCR, immunohistochemistry, and Western blotting. The proliferation, migration, and invasion of ectopic endometrial epithelial cells and Ishikawa cells were evaluated by MTT, EdU, wound healing, and transwell assays. Inflammatory cytokine levels were detected by ELISA. Luciferase assays were used to measure activity of the ZEB1 promoter site pGL3-P886. 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. 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.

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Condition tags

endometriosis

MeSH descriptors

Endometrial Neoplasms Endometriosis Endometrium Epithelial Cells Promoter Regions, Genetic RNA, Long Noncoding Zinc Finger E-box-Binding Homeobox 1 Animals Cell Line, Tumor Cell Proliferation Endometrial Neoplasms Endometriosis Endometriosis Endometrium Epithelial Cells Epithelial-Mesenchymal Transition Epithelial-Mesenchymal Transition Female Gene Expression Regulation, Neoplastic Humans

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