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

Qin Yu, Jianzhang Wang, Tiantian Li, Xinyue Guo, Shaojie Ding, Xuan Che, Libo Zhu, Yangying Peng, Xinxin Xu, Gen Zou, Xinmei Zhang
Journal of cellular and molecular medicine · 2021 · vol. 25(3) , pp. 1601–1612 · doi:10.1111/jcmm.16261 · PMID:33410267 · W3120707758
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Receptor d'origine nantais (RON) activation promotes epithelial-mesenchymal transition in endometrial epithelial cells through Akt and MAPK pathways, contributing to endometriosis development and lesion formation in mice.

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Abstract

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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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Disease Susceptibility Endometriosis Endometriosis Epithelial Cells Epithelial-Mesenchymal Transition Receptor Protein-Tyrosine Kinases Biomarkers Cell Movement Endometriosis Endometriosis Epithelial Cells Epithelial Cells Female Humans Immunohistochemistry Mitogen-Activated Protein Kinases Mitogen-Activated Protein Kinases Proto-Oncogene Proteins c-akt Proto-Oncogene Proteins c-akt Receptor Protein-Tyrosine Kinases

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