Journal
ACTA OBSTETRICIA ET GYNECOLOGICA SCANDINAVICA
Volume 96, Issue 9, Pages 1128-1135Publisher
WILEY
DOI: 10.1111/aogs.13179
Keywords
Endometriosis; epithelial-mesenchymal transition; ZEB1; Snail; E-cadherin; vimentin; CA125
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Funding
- Japan Society for the Promotion of Science [16K11108]
- Cell Science Research Foundation
- Takeda Science foundation
- Grants-in-Aid for Scientific Research [16K11110, 17K19731, 16K11109, 17K11251, 16K11108, 16H05474] Funding Source: KAKEN
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IntroductionAlthough endometriosis is a benign disease, it shares some features with cancers, such as invasiveness and the potential to metastasize. This study sought to investigate the epithelial-mesenchymal transition status in human endometriotic lesions. Material and methodsThirteen endometriosis patients and 10 control women without endometriosis undergoing surgery for benign indications were recruited. We examined the expression of E-cadherin, vimentin, and epithelial-mesenchymal transition-induced transcriptional factors, such as Snail and ZEB1, by immunohistochemistry. We evaluated the expression of each marker in epithelial cells of both endometriotic lesions (ovarian endometrioma, deep infiltrating endometriosis, adenomyosis) and normal endometria. The correlation between ZEB1 expression and serum level of CA125 was also investigated. ResultsImmunohistochemical analysis revealed that although E-cadherin, vimentin, and Snail were expressed in epithelia of normal endometria and endometriotic lesions, ZEB1 expression was only expressed in epithelia of endometriotic lesions. Additionally, ZEB1 was most frequently observed in epithelial cells of invasive endometriosis. The endometriosis patients with high serum CA125 level were more likely to have ZEB1-positive lesions. ConclusionsThis is the first observation of ZEB1 expression in epithelial cells of benign disease. The preferential expression of ZEB1 in epithelial cells of endometriotic lesions suggests that these cells may have, at least in part, a higher level of mesenchymal features possibly via ZEB1-driven epithelial-mesenchymal transition than normal endometria and that ZEB1 can be a potential indicator of invasiveness or severity of endometriosis.
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