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Published online: 2021-07-16
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Endoglin promotes cell migration and invasion in endometriosis by regulating EMT

Xiutang Chen, Junjian Wang, Feixia Tu, Qing Yang, Dan Wang, Qin Zhu
DOI: 10.5603/GP.a2021.0130

open access

Ahead of Print
ORIGINAL PAPERS Gynecology
Published online: 2021-07-16

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.

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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Keywords

endometriosis; endoglin; epithelial to mesenchymal transition

About this article
Title

Endoglin promotes cell migration and invasion in endometriosis by regulating EMT

Journal

Ginekologia Polska

Issue

Ahead of Print

Article type

Research paper

Published online

2021-07-16

DOI

10.5603/GP.a2021.0130

Keywords

endometriosis
endoglin
epithelial to mesenchymal transition

Authors

Xiutang Chen
Junjian Wang
Feixia Tu
Qing Yang
Dan Wang
Qin Zhu

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