The Possible Role of Eukaryotic Translation Initiation Factor 3 Subunit e (eIF3e) in the Epithelial—Mesenchymal Transition in Adenomyosis

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Decreased eIF3e expression in adenomyosis ectopic endometrium correlates with increased EMT markers and may activate TGF-β1 signaling, suggesting a role in adenomyosis development.

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This study examined whether eukaryotic translation initiation factor 3 subunit e (eIF3e) is involved in epithelial–mesenchymal transition (EMT) in adenomyosis by comparing immunohistochemistry markers in ectopic endometrial tissue from 40 premenopausal women with ultrasonographically diagnosed and histologically confirmed adenomyosis versus endometrium from 40 cycling premenopausal controls without endometriosis, adenomyosis, or uterine fibroids. The adenomyosis group showed reduced immunoreactivity for eIF3e and E-cadherin, alongside increased immunoreactivity for TGF-β1, Snail, vimentin, and PCNA, with these differences not influenced by age, parity, or menstrual phase, and eIF3e levels correlating negatively with several EMT-associated markers. A key limitation is that the findings are based on tissue staining and correlation, without functional experiments demonstrating causal regulation of EMT by eIF3e or TGF-β1 signaling. This paper is centrally about endometriosis and adenomyosis — it specifically investigates eIF3e’s role in EMT processes in adenomyosis tissue.

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Abstract

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. Similar content being viewed by others

References

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adenomyosis

MeSH descriptors

Adenomyosis Endometrium Epithelial-Mesenchymal Transition Eukaryotic Initiation Factor-3 Adenomyosis Adult Cell Proliferation Endometrium Eukaryotic Initiation Factor-3 Female Humans Middle Aged Signal Transduction Transforming Growth Factor beta1 Transforming Growth Factor beta1

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