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.
Highlights
Endometriosis, characterized by existence of endometrial‐like tissue outside of the uterine cavity, mainly causes chronic pelvic pain and infertility in women of reproductive years.[1]
We propose that the β‐catenin/Snail interaction plays an important role in oestrogen‐induced Epithelial‐mesenchymal transition (EMT) in epithelial cells (EECs) and contributes to the development of ovarian endometriosis
Down‐regulated E‐cadherin expression and up‐regulated vimentin expression were observed in the epithelial cells of ovarian endome‐ triotic tissues, and the alternations of these EMT markers were re‐ lated with E2 treatment
Summary
Endometriosis, characterized by existence of endometrial‐like tissue outside of the uterine cavity, mainly causes chronic pelvic pain and infertility in women of reproductive years.[1]. Mation of adhesion and clinical symptoms, such as pelvic pain and infertility.[12] oestrogen was shown to induce EMT in many dis‐ eases.[13,14,15] In human prostate cancer cell lines, oestrogen signalling could induce EMT and promote osteoblastic tumour formation.[16] In. Xiong and Zhang should be regarded as joint First Authors. The loss of E‐cadherin can further promote β‐catenin release from cytomembrane and activation.[25,26] Our recent research discovered that oestrogen induced high expression of β‐catenin in human endometrial stromal cells of ectopic endometrium, which increased cellular invasion and angiogenesis.[27,28] And the role of oestrogen on the EMT process of human endometrial epithelial cells remains unknown. Β‐catenin signalling acti‐ vating Snail promoter functions a crucial role in oestrogen‐facilitated migration and invasion in endometrial epithelial cells
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