E2‐mediated EMT by activation of β‐catenin/Snail signalling during the development of ovarian endometriosis

Wenqian Xiong, Ling Zhang, Hengwei Liu, Na Li, Yu Du, Haitang He, Zhibing Zhang, Yi Liu
Journal of cellular and molecular medicine · 2019 · vol. 23(12) , pp. 8035–8045 · doi:10.1111/jcmm.14668 · PMID:31560827 · W2976436811
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Oestradiol exposure promotes ovarian endometriosis development by activating β-catenin/Snail signalling, which drives epithelial-mesenchymal transition in endometrial epithelial cells.

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Abstract

Endometriosis is an oestrogen-dependent disease, and epithelial-mesenchymal transition (EMT) is involved in the process of endometriosis. Whether oestrogen could induce EMT in endometriosis remains largely unknown. Here, we reported that up-regulated expression of EMT markers in ovarian chocolate cyst is accompanied by high expression 17β-hydroxysteroid dehydrogenase 1 (17β-HSD1), and exposure of primary human endometrial epithelial cells to oestradiol conditions could promote EMT occurrence and activate both β-catenin and Snail signalling. Furthermore, we found nuclear β-catenin and Snail expression was closely linked in ovarian endometriosis, and β-catenin knockdown abrogated oestrogen-induced Snail mediated EMT in vitro. This is due to that β-catenin/ TCF-3 could bind to Snail promoter and activate its transcription. These results suggested that β-catenin signalling functions as the Snail activator and plays a critical role in oestradiol-induced EMT in endometriosis.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

beta Catenin Endometriosis Epithelial-Mesenchymal Transition Epithelial-Mesenchymal Transition Estradiol Ovarian Cysts Snail Family Transcription Factors 17-Hydroxysteroid Dehydrogenases 17-Hydroxysteroid Dehydrogenases Adult beta Catenin Cadherins Cadherins Cell Movement Cell Movement Cells, Cultured Chromatin Immunoprecipitation Endometriosis Endometriosis Endometrium

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 (56)

Cited by (50)

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