Endoglin promotes cell migration and invasion in endometriosis by regulating EMT.

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.