期刊
GYNECOLOGIC AND OBSTETRIC INVESTIGATION
卷 84, 期 5, 页码 485-494出版社
KARGER
DOI: 10.1159/000499625
关键词
Forkhead box protein M1; Epithelial-mesenchymal transition; Endometriosis; Snail
Aim: The aim of this study was to investigate the expression of Forkhead box M1 (FoxM1) in endometriosis and determine FoxM1's possible effects on endometriotic epithelial cells (EECs) invasion and epithelial-mesenchymal transition (EMT). Methods: The expression of FoxM1 and E-cadherin in endometrium and ectopic tissues was analyzed by immunohistochemistry. The transforming growth factor-beta 1 (TGF-beta 1) was added to induce EMT of EECs, which were purified from ectopic tissues. The Short hairpin RNA (ShRNA) intervention technique was used to silence FoxM1. The morphological changes of EECs were observed by microscope. The invasion ability of EECs was determined by transwell invasion assay. The expression of FoxM1 and EMT-related gene (E-cadherin, N-cadherin, vimentin, and Snail) in EECs was detected by quantitative reverse transcription-polymerase chain reaction and western blot. Results: FoxM1 expression was significantly increased, while E-cadherin expression was significantly decreased in ectopic tissues than that in endometrium tissues. After TGF-beta 1 treatment, EECs showed a transformation from an epithelial sheet-like structure to a mesenchymal fibroblastic spindle shape; EECs invasion ability was enhanced; the level changes of EMT-related molecule also indicated an EMT phenotype of EECs. After FoxM1-shRNA intervention, TGF-beta 1-induced changes of EECs in morphology, invasion ability and EMT-related molecule expressions were partially reversed. Conclusions: Silencing of FoxM1 could reverse TGF-beta 1-induced invasion and EMT of EECs.
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