RhoA/ROCK pathway mediates the effect of oestrogen on regulating epithelial‐mesenchymal transition and proliferation in endometriosis

Zhi-Xiong Huang, Zhixiong Huang, Xiao‐Mei Mao, Xiao-Mei Mao, Rong-Feng Wu, Rongfeng Wu, Shaomin Huang, Shao-Min Huang, Xin-Yu Ding, Xinyu Ding, Qionghua Chen, Qiong-Hua Chen, Qing‐Xi Chen
Journal of cellular and molecular medicine · 2020 · vol. 24(18) , pp. 10693–10704 · doi:10.1111/jcmm.15689 · W3045618018
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⚙ AI-generated summary by claude@2026-06, 2026-06-09 ⓘ

This study found that the RhoA/ROCK pathway is abnormally activated in endometriosis, mediating the effects of estrogen and ERα signaling on epithelial-mesenchymal transition and proliferation.

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Abstract

Abstract Endometriosis is a benign gynaecological disease appearing with pelvic pain, rising dysmenorrhoea and infertility seriously impacting on 10% of reproductive‐age females. This research attempts to demonstrate the function and molecular mechanism of RhoA/ROCK pathway on epithelial‐mesenchymal transition (EMT) and proliferation in endometriosis. The expression of Rho family was abnormally changed in endometriotic lesions; in particular, RhoA and ROCK1/2 were significantly elevated. Overexpression of RhoA in human eutopic endometrial epithelial cells (eutopic EECs) enhanced the cell mobility, epithelial‐mesenchymal transition (EMT) and proliferation, and RhoA knockdown exhibited the opposite function. Oestrogen up‐regulated the RhoA activity and expression of RhoA and ROCK1/2. RhoA overexpression reinforced the effect of oestrogen on promoting EMT and proliferation, and RhoA knockdown impaired the effect of oestrogen. oestrogen receptor α (ERα) was involved with the regulation of oestrogen on EMT and proliferation and up‐regulated RhoA activity and expression of RhoA and ROCK1/2. The function of ERα was modulated by the change in RhoA expression. Furthermore, phosphorylated ERK that was enhanced by oestrogen and ERα promoted the protein expression of RhoA/ROCK pathway. Endometriosis mouse model revealed that oestrogen enhanced the size and weight of endometriotic lesions. The expression of RhoA and phosphorylated ERK in mouse endometriotic lesions was significantly elevated by oestrogen. We conclude that abnormal activated RhoA/ROCK pathway in endometriosis is responsible for the function of oestrogen/ERα/ERK signalling, which promoted EMT and proliferation and resulted in the development of endometriosis.

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Condition tags

mesh:D004715endometriosisdysmenorrheainfertility

MeSH descriptors

Endometriosis Endometrium Epithelial-Mesenchymal Transition Estrogens rhoA GTP-Binding Protein rho-Associated Kinases Signal Transduction Adult Animals Cells, Cultured Disease Models, Animal Endometriosis Endometriosis Endometrium Endometrium Endometrium Epithelial-Mesenchymal Transition Epithelial-Mesenchymal Transition Estradiol Estradiol

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (41)

Cited by (36)

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