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Recepteur d'origine nantais contributes to the development of endometriosis via promoting epithelial‐mesenchymal transition of a endometrial epithelial cells

Endometriosis is a benign, chronic inflammatory disease that commonly occurs in reproductive‐aged women. Epithelial‐mesenchymal transition (EMT) of endometrial epithelial cells plays an important role in the development of endometriosis. Recepteur d'origine nantais (RON), a receptor tyrosine ki...

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Autores principales: Yu, Qin, Wang, Jianzhang, Li, Tiantian, Guo, Xinyue, Ding, Shaojie, Che, Xuan, Zhu, Libo, Peng, Yangying, Xu, Xinxin, Zou, Gen, Zhang, Xinmei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7875913/
https://www.ncbi.nlm.nih.gov/pubmed/33410267
http://dx.doi.org/10.1111/jcmm.16261
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author Yu, Qin
Wang, Jianzhang
Li, Tiantian
Guo, Xinyue
Ding, Shaojie
Che, Xuan
Zhu, Libo
Peng, Yangying
Xu, Xinxin
Zou, Gen
Zhang, Xinmei
author_facet Yu, Qin
Wang, Jianzhang
Li, Tiantian
Guo, Xinyue
Ding, Shaojie
Che, Xuan
Zhu, Libo
Peng, Yangying
Xu, Xinxin
Zou, Gen
Zhang, Xinmei
author_sort Yu, Qin
collection PubMed
description Endometriosis is a benign, chronic inflammatory disease that commonly occurs in reproductive‐aged women. Epithelial‐mesenchymal transition (EMT) of endometrial epithelial cells plays an important role in the development of endometriosis. Recepteur d'origine nantais (RON), a receptor tyrosine kinase, has been reported to promote EMT and progression in tumours. However, whether and how RON mediates the EMT and endometriosis development is not known. Here, we found that RON activation could improve the migratory and invasive capabilities, change cellular morphologies, and decrease expression of E‐cadherin and increase expression of N‐cadherin in endometrial epithelial cells. Inhibition or knockdown of RON expression suppressed the migration and invasion of endometrial epithelial cells. Our studies also indicated that RON played its part in endometrial epithelial cells through protein kinase B (Akt) and mitogen‐activated protein kinase (MAPK) pathways. Treatment with a RON inhibitor could decrease the number of ectopic lesions in a mouse model of endometriosis and mediate expression of EMT markers in endometriotic lesions. These data suggest that RON contributed to endometriosis development by promoting EMT of endometrial epithelial cells. Therefore, RON may be a new therapeutic target for endometriosis.
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spelling pubmed-78759132021-02-18 Recepteur d'origine nantais contributes to the development of endometriosis via promoting epithelial‐mesenchymal transition of a endometrial epithelial cells Yu, Qin Wang, Jianzhang Li, Tiantian Guo, Xinyue Ding, Shaojie Che, Xuan Zhu, Libo Peng, Yangying Xu, Xinxin Zou, Gen Zhang, Xinmei J Cell Mol Med Original Articles Endometriosis is a benign, chronic inflammatory disease that commonly occurs in reproductive‐aged women. Epithelial‐mesenchymal transition (EMT) of endometrial epithelial cells plays an important role in the development of endometriosis. Recepteur d'origine nantais (RON), a receptor tyrosine kinase, has been reported to promote EMT and progression in tumours. However, whether and how RON mediates the EMT and endometriosis development is not known. Here, we found that RON activation could improve the migratory and invasive capabilities, change cellular morphologies, and decrease expression of E‐cadherin and increase expression of N‐cadherin in endometrial epithelial cells. Inhibition or knockdown of RON expression suppressed the migration and invasion of endometrial epithelial cells. Our studies also indicated that RON played its part in endometrial epithelial cells through protein kinase B (Akt) and mitogen‐activated protein kinase (MAPK) pathways. Treatment with a RON inhibitor could decrease the number of ectopic lesions in a mouse model of endometriosis and mediate expression of EMT markers in endometriotic lesions. These data suggest that RON contributed to endometriosis development by promoting EMT of endometrial epithelial cells. Therefore, RON may be a new therapeutic target for endometriosis. John Wiley and Sons Inc. 2021-01-06 2021-02 /pmc/articles/PMC7875913/ /pubmed/33410267 http://dx.doi.org/10.1111/jcmm.16261 Text en © 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Yu, Qin
Wang, Jianzhang
Li, Tiantian
Guo, Xinyue
Ding, Shaojie
Che, Xuan
Zhu, Libo
Peng, Yangying
Xu, Xinxin
Zou, Gen
Zhang, Xinmei
Recepteur d'origine nantais contributes to the development of endometriosis via promoting epithelial‐mesenchymal transition of a endometrial epithelial cells
title Recepteur d'origine nantais contributes to the development of endometriosis via promoting epithelial‐mesenchymal transition of a endometrial epithelial cells
title_full Recepteur d'origine nantais contributes to the development of endometriosis via promoting epithelial‐mesenchymal transition of a endometrial epithelial cells
title_fullStr Recepteur d'origine nantais contributes to the development of endometriosis via promoting epithelial‐mesenchymal transition of a endometrial epithelial cells
title_full_unstemmed Recepteur d'origine nantais contributes to the development of endometriosis via promoting epithelial‐mesenchymal transition of a endometrial epithelial cells
title_short Recepteur d'origine nantais contributes to the development of endometriosis via promoting epithelial‐mesenchymal transition of a endometrial epithelial cells
title_sort recepteur d'origine nantais contributes to the development of endometriosis via promoting epithelial‐mesenchymal transition of a endometrial epithelial cells
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7875913/
https://www.ncbi.nlm.nih.gov/pubmed/33410267
http://dx.doi.org/10.1111/jcmm.16261
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