open access
Endoglin promotes cell migration and invasion in endometriosis by regulating EMT
Affiliations- People's Hospital of AnJi, Dipu Town, Anji County, Huzhou, China
- Zhejiang Cancer Hospital, Hangzhou, China
open access
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.
Keywords
endometriosis; endoglin; epithelial to mesenchymal transition
About this articleTitle
Endoglin promotes cell migration and invasion in endometriosis by regulating EMT
Journal
Issue
Article type
Research paper
Published online
2021-07-16
Page views
1418
Article views/downloads
930
DOI
Pubmed
Keywords
endometriosis
endoglin
epithelial to mesenchymal transition
Authors
Xiutang Chen
Junjian Wang
Feixia Tu
Qing Yang
Dan Wang
Qin Zhu
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