Oestrogen-induced epithelial-mesenchymal transition (EMT) in endometriosis: Aetiology of vaginal agenesis in Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome
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⤵ 24 in-corpus citations
Abstract
Endometriosis occurs when endometrial-like tissue forms and grows outside the uterus due to oestrogen-induced epithelial-mesenchymal transition in the female reproductive tract. Factors that suppress this event could become potential therapeutic agents against disease occurrence and progression. However, an overview of these studies is still lacking. This review assessed the impact of a number factors on oestrogen-mediated epithelial-mesenchymal transition in the emergence of several diseases in the female reproductive tract, primarily endometriosis. The association between epithelial-mesenchymal transition and Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome was also investigated. Oestrogen, Wnt4 and epithelial-mesenchymal transition were chosen as keywords in Scopus, PubMed, and Web of Science searches performed on 28th June 2021. Study selection was refined to cancer-irrelevant, English, original articles published between years 2011-2021. The full-text assessment was carried out for topic-related articles after title and abstract screening. Included studies were summarised and assessed for their risk of bias using the Office of Health Assessment and Translation tool. In this review, 10 articles investigating oestrogen and epithelial-mesenchymal transition in the female reproductive tract were summarised and classified into two groups: seven studies under 'factor'-modulated epithelial-mesenchymal transition and three studies under 'factor'-manipulated oestrogen-induced epithelial-mesenchymal transition. The current evidence proposes that epithelial-mesenchymal transition is one of the prime causes of reproductive-related disease. This event could be mediated by distinct stimuli, specifically oestrogen and Wnt4 aberration. The results of this review suggest that oestrogen and Wnt4 participate in epithelial-mesenchymal transition in vaginal epithelial cells in MRKH syndrome, adopting from the theories of endometriosis development, which could therefore serve as a foundation for novel target treatment, specifically related to vaginal epithelialisation, to ensure better surgical outcomes.
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References (78)
- Bioinformatic analysis reveals the importance of epithelial-mesenchymal transition in the development of endometriosis via openalex
- Downregulated circular RNA hsa_circ_0067301 regulates epithelial-mesenchymal transition in endometriosis via the miR-141/Notch signaling pathway via openalex
- Endometriosis and breast cancer: A survey of the epidemiological studies via openalex
- Endometriosis: A Role for Stem Cells via openalex
- Enhanced epithelial to mesenchymal transition (EMT) and upregulated MYC in ectopic lesions contribute independently to endometriosis via openalex
- Epithelial-to-mesenchymal transition in the development of endometriosis via openalex
- Epithelial-to-Mesenchymal Transition in the Female Reproductive Tract: From Normal Functioning to Disease Pathology via openalex
- Estradiol promotes EMT in endometriosis via MALAT1/miR200s sponge function via openalex
- Estrogen attenuates TGF-β1-induced EMT in intrauterine adhesion by activating Wnt/β-catenin signaling pathway via openalex
- Estrogen Receptor (ER) β Regulates ERα Expression in Stromal Cells Derived from Ovarian Endometriosis via openalex
- Expression of estrogen receptor alpha and beta in peritoneal and ovarian endometriosis via openalex
- High-Expression of Neuropilin 1 Correlates to Estrogen-Induced Epithelial-Mesenchymal Transition of Endometrial Cells in Adenomyosis via openalex
- High expression of ZEB1 in endometriosis and its role in 17β-estradiol-induced epithelial-mesenchymal transition. via openalex
- LINC01541 overexpression attenuates the 17β-Estradiol-induced migration and invasion capabilities of endometrial stromal cells via openalex
- Lipoxin A4 Suppresses Estrogen-Induced Epithelial-Mesenchymal Transition via ALXR-Dependent Manner in Endometriosis via openalex
- Long non‐coding RNA AFAP1‐AS1 promoting epithelial‐mesenchymal transition of endometriosis is correlated with transcription factor ZEB1 via openalex
- Melatonin inhibits 17β-estradiol-induced migration, invasion and epithelial-mesenchymal transition in normal and endometriotic endometrial epithelial cells via openalex
- miR-200c suppresses endometriosis by targeting MALAT1 in vitro and in vivo via openalex
- Oestrogen induces epithelial‐mesenchymal transition in endometriosis via circ_0004712/miR‐148a‐3p sponge function via openalex
- Origin of endometriosis from the mesenchyme of the celomic walls via openalex
- Pathogenomics of Endometriosis Development via openalex
- Recepteur d'origine nantais contributes to the development of endometriosis via promoting epithelial‐mesenchymal transition of a endometrial epithelial cells via openalex
- RhoA/ROCK pathway mediates the effect of oestrogen on regulating epithelial‐mesenchymal transition and proliferation in endometriosis via openalex
- The expression of estrogen receptors as well as GREB1, c-MYC, and cyclin D1, estrogen-regulated genes implicated in proliferation, is increased in peritoneal endometriosis via openalex
- ZEB1 expression is a potential indicator of invasive endometriosis via openalex
- W2179586681 via openalex
- W2215200760 via openalex
- W2260083591 via openalex
- W2336099036 via openalex
- W2489222159 via openalex
- W2525370412 via openalex
- W2528855361 via openalex
- W2552015768 via openalex
- W2746805351 via openalex
- W2755064547 via openalex
- W2767452831 via openalex
- W2810203177 via openalex
- W2884618837 via openalex
- W2902522405 via openalex
- W2941873727 via openalex
- W2943218794 via openalex
- W2956663640 via openalex
- W2973987577 via openalex
- W3012664161 via openalex
- W3026492968 via openalex
- W3045550416 via openalex
- W3092434283 via openalex
- W3093525518 via openalex
- W3094771245 via openalex
- W3114122775 via openalex
- W3134440229 via openalex
- W6685865761 via openalex
- W44000797 via openalex
- W6773668886 via openalex
- W1498970130 via openalex
- W1866220599 via openalex
- W1963501822 via openalex
- W1964081206 via openalex
- W1964847767 via openalex
- W1976751554 via openalex
- W2019379578 via openalex
- W2020490350 via openalex
- W2020617101 via openalex
- W2029915978 via openalex
- W2037561079 via openalex
- W2041369790 via openalex
- W2044651071 via openalex
- W2052041317 via openalex
- W2053340664 via openalex
- W2063581615 via openalex
- W2072503088 via openalex
- W2085707729 via openalex
- W2116888004 via openalex
- W2122038030 via openalex
- W2129910915 via openalex
- W2133799748 via openalex
- W2154589460 via openalex
- W2171875732 via openalex
Cited by (24)
- Integrated analysis of single-cell and bulk transcriptomic data reveals altered cellular composition and predictive cell types in ectopic endometriosis 2025
- TGF-β/snail-mediated epithelial-to-mesenchymal transition disrupts estradiol metabolism through suppressing the HSD17B2 expression in endometriotic epithelial cells 2025
- Additional file 9 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 5 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 1 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 2 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 6 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 4 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 1 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 8 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 6 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 9 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 7 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 3 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 4 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 5 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 2 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 7 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 8 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Endometriosis: Pathogenesis, Diagnosis and Treatment, volume II 2024
- Celecoxib attenuates interleukin 33-induced expression of vascular cell adhesion molecule-1 in human ovarian endometriotic stromal cells 2024
- Environmental Exposure to Persistent Organic Pollutants and Its Association with Endometriosis Risk: Implications in the Epithelial–Mesenchymal Transition Process 2024
- The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
- Additional file 3 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin 2024
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