Endoglin promotes cell migration and invasion in endometriosis by regulating EMT

Xiutang Chen, Junjian Wang, Feixia Tu, Fei-xia Tu, Qing Yang, Dan Wang, Qin Zhu
Ginekologia polska · 2021 · vol. 95(9) , pp. 661–667 · doi:10.5603/gp.a2021.0130 · PMID:34541637 · W3183545098
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Abstract

OBJECTIVES: This study aims to investigate the expression and role of Endoglin (ENG) in endometriosis (EM). MATERIAL AND METHODS: In this study, quantitative real-time polymerase chain reaction, western blot and immunohistochemistry were used to examine the expression of ENG in tissues. Cellular experiments were performed to evaluate the effect of ENG on cellular biological function. Western blot was used to examine the expression of epithelial to mesenchymal transition-related proteins. RESULTS: The expression of ENG was significantly higher in the ectopic endometriotic tissues than that in eutopic endometriotic tissues. Knockdown of ENG inhibited cell viability, migration and invasion, and induced cell apoptosis in hEM15A cells. Additionally, silenced ENG caused increased levels of E-cadherin and decreased levels of N-cadherin, vimentin, MMP-2 and MMP-9. CONCLUSIONS: These results confirmed that ENG may be involved in the development of endometriosis by promoting EMT process, revealing a new insight into the pathogenesis of endometriosis and contributing to the exploration of molecular therapeutic strategies against endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Cell Movement Endoglin Endoglin Endoglin Endometriosis Endometriosis Endometriosis Endometriosis Epithelial-Mesenchymal Transition Adult Apoptosis Cadherins Cadherins Female Humans

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