Open AccessE 2 ‐mediated EMT by activation of β‐catenin/Snail signalling during the development of ovarian endometriosis
Author(s) -
Xiong Wenqian,
Zhang Ling,
Liu Hengwei,
Li Na,
Du Yu,
He Haitang,
Zhang Zhibing,
Liu Yi
Publication year - 2019
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.14668
Subject(s) - snail , endometriosis , gene knockdown , epithelial–mesenchymal transition , catenin , cancer research , biology , transcription factor , medicine , microbiology and biotechnology , signal transduction , cancer , apoptosis , wnt signaling pathway , metastasis , gene , ecology , biochemistry
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.