Epithelial-mesenchymal transition (EMT) has been reported to be involved in adenomyosis by promoting cell invasion and fibrogenesis. But few studies have identified critical factors that regulate EMT process during adenomyosis. The eukaryotic translation initiation factor 3 subunit e (eIF3e) protein is a component of the multisubunit eIF3 complex essential for cap-dependent translation initiation. The aim of this study was to investigate whether eIF3e is involved in EMT in adenomyosis. Ectopic endometrial tissue samples were collected from 40 premenopausal women with ultrasonographically diagnosed and histologically confirmed adenomyosis. As controls, endometrial samples were obtained from 40 cycling premenopausal women patients who underwent surgery for benign gynecologic disorders or cervical intraepithelial neoplasia but without endometriosis, adenomyosis, nor uterine fibroids. All tissue samples were subjected to immunohistochemistry analysis of eIF3e, transforming growth factor-β1 (TGF-β1), E-cadherin, vimentin, Snail, and proliferating cell nuclear antigen (PCNA). The epithelial component of ectopic endometrium showed significantly reduced immunoreactivity against eIF3e and E-cadherin but elevated immunoreactivity against TGF-β1, Snail, vimentin, and PCNA as compared with that of control endometrium (all P values <.05), and the difference was not affected by age, parity, or menstrual phase. The eIF3e staining levels correlated negatively with those of TGF-β1, vimentin, Snail, and PCNA (both P values <.05). These data suggest that decreased eIF3e expression may pave way for EMT in the development of adenomyosis through activating the TGF-β1 signaling pathway. Our study provided novel insights into the development and treatments of adenomyosis.
Keywords: TGF-β1; adenomyosis; eIF3e; epithelial–mesenchymal transition.