Differential expression of EWI‐2 in endometriosis, its functional role and underlying molecular mechanisms

Tingting Zheng, Jing Yang
Journal of Obstetrics and Gynaecology Research · 2017 · vol. 43(7) , pp. 1180–1188 · doi:10.1111/jog.13333 · PMID:28544021 · W2617655324
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EWI-2 was downregulated in endometriosis tissues and inhibited cell migration and invasion via the Akt signaling pathway, suggesting it is a potential diagnostic biomarker.

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Abstract

Abstract Aim We aimed to investigate EWI‐2 expression in endometrium tissues collected from women with endometriosis at mRNA and protein levels, to evaluate its potential as a biomarker for endometriosis and to study its functional role via possible regulation of the PI3K/Akt signaling pathway. Methods Endometrium tissues were collected from patients with endometriosis and healthy individuals. EWI‐2 mRNA expression was evaluated using quantitative real‐time PCR (qRT‐PCR) while EWI‐2 protein levels were determined by western blotting. For functional studies, EWI‐2 shRNA was transfected in endometrial epithelial cells and the in vitro migration and invasion assays were performed using the Transwell chambers. Results EWI‐2 was significantly downregulated in tissues obtained from patients with endometriosis compared with healthy individuals ( P < 0.0001). EWI‐2 expression in the secretory phase was lower than that in the proliferative phase ( P < 0.0001). Receiver–operator curve analysis of EWI‐2 expression showed that the area under the curve for endometriosis diagnosis was 0.8942 ( P = 0.003), 0.9643 ( P = 0.0001), 0.9912 ( P < 0.0001), and 0.9150 ( P < 0.0001), respectively, for healthy women compared with women with endometriosis in matched comparisons of data originated from the proliferative, early, middle, and late secretory phases. Over the menstrual cycle, the expression of EWI‐2 was significantly decreased in the eutopic tissues compared to the ectopic tissues. Further cellular and molecular analyses showed that EWI‐2 inhibited cell migration and invasion via the Akt signaling. Conclusion Our findings suggested that downregulation of EWI‐2 may contribute to endometriosis physiopathology and potentiate EWI‐2 as a valuable diagnostic biomarker and therapeutic target for endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Antigens, CD Endometriosis Membrane Proteins Adult Antigens, CD Biomarkers Cell Culture Techniques Endometriosis Endometriosis Female Humans Membrane Proteins Middle Aged Young Adult

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