Epithelial-to-mesenchymal transition in the development of endometriosis

Yan-Meng Yang, Yanmeng Yang, Wan-Xi Yang, Wan‐Xi Yang
Oncotarget · 2017 · vol. 8(25) , pp. 41679–41689 · doi:10.18632/oncotarget.16472 · PMID:28415639 · PMC5522315 · W2603106635
review OA: gold CC0 ⤵ 117 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review explores how epithelial-to-mesenchymal transition, activated by hypoxia and estrogen through various pathways, contributes to endometriosis development and lesion formation.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-08 ⓘ

This paper reviews the hypothesis that epithelial-to-mesenchymal transition (EMT) contributes to endometriosis development, drawing on evidence from prior studies that ectopic endometrial cells show downregulated epithelial markers (e.g., E-cadherin, occludin) and upregulated mesenchymal markers (e.g., vimentin, N-cadherin), which is associated with invasion and anoikis resistance. It highlights that EMT is typically categorized into three biological types (developmental, injury/inflammation-driven fibrosis, and tumor-like metastatic programs) and proposes that chronic injury/fibrosis and inflammatory features of endometriosis may align with Type 2 EMT, while metastasis-associated behavior and angiogenesis may align with Type 3 EMT. The review further discusses two proposed EMT-inducing stimuli in endometriosis—hypoxia (via HIF-1α and VEGF pathways, ROS, and hypoxia-linked EMT factors including TGF-β) and estrogen—while acknowledging that detailed EMT “signals” and the exact EMT subtype(s) in endometriotic cells are not well established. This paper is centrally about endometriosis — it argues that EMT, potentially including specific EMT types, underlies the development and progression of endometriotic lesions.

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Abstract

// Yan-Meng Yang 1 and Wan-Xi Yang 1 1 The Sperm Laboratory, College of Life Sciences, Zhejiang University, Hangzhou, China Correspondence to: Wan-Xi Yang, email: // Keywords : epithelial-to-mesenchymal transition, endometriosis, infertility Received : January 25, 2017 Accepted : March 11, 2017 Published : March 22, 2017 Abstract Endometriosis, an estrogen-dependent chronic gynecological disease, is common in reproductive-age women and profoundly affects their life quality. Although various pathogenic theories have been proposed, the origin of endometriosis remains unclear. Epithelial to mesenchymal transition (EMT) is a process that epithelial cells lose polarized organization of the cytoskeleton and cell-to-cell contacts, acquiring the high motility of mesenchymal cells. These changes are thought to be prerequisites for the original establishment of endometriotic lesions. However, no study exactly indicates which type of EMT occurs in endometriosis. In this review, we conclude that two different types of EMT may participate in this disease. Besides, two stimulating signals, hypoxia and estrogen, can through different pathways to activate the EMT process in endometriosis. Those pathways involve many cellular factors such as TGF-beta and Wnt, ultimately leading to cell proliferation and migration. As infertility is becoming a serious and intractable issue for women, EMT, during the implantation process, is gaining attention. In this review, we will describe the known functions of EMT in endometriosis, and suggest further studies that may aid in the development of medical therapy.

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Condition tags

endometriosisinfertility

MeSH descriptors

Endometriosis Epithelial-Mesenchymal Transition Infertility Endometriosis Endometriosis Epithelial-Mesenchymal Transition Estrogens Estrogens Female Humans Infertility Infertility

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