The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Oestrogen‐induced epithelial–mesenchymal transition of endometrial epithelial cells contributes to the development of adenomyosis
Open accessAbstract
Adenomyosis is an oestrogen‐dependent disease caused by a downward extension of the endometrium into the uterine myometrium. Epithelial–mesenchymal transition (EMT) endows cells with migratory and invasive properties and can be induced by oestrogen. We hypothesized that oestrogen‐induced EMT is critical in the pathogenesis of adenomyosis. We first investigated whether EMT occurred in adenomyotic lesions and whether it correlated with serum 17β‐oestradiol (E2) levels. Immunohistochemistry was performed on adenomyotic lesions and corresponding eutopic endometrium samples from women with adenomyosis. Endometria from women without endometrial disorders were used as a control. In the epithelial component of adenomyotic lesions, vimentin expression was up‐regulated and E‐cadherin expression was down‐regulated compared to the eutopic endometrium, suggesting that EMT occurs in adenomyosis. In adenomyosis, the serum E2 level was negatively correlated with E‐cadherin expression in the epithelial components of the eutopic endometrium and adenomyotic lesions, suggesting the involvement of oestrogen‐induced EMT in endometrial cells. In oestrogen receptor‐positive Ishikawa endometrial epithelial cells, oestrogen induced a morphological change to a fibroblast‐like phenotype, a shift from epithelial marker expression to mesenchymal marker expression, increased migration and invasion, and up‐regulation of the EMT regulator Slug. Raloxifene, a selective oestrogen receptor modulator, abrogated these effects. To determine the role of oestrogen‐induced EMT in the implantation of ectopic endometrium, we xenotransplanted eutopic endometrium or adenomyotic lesions from adenomyosis patients into ovariectomized SCID mice. The implantation of endometrium was oestrogen‐dependent and was suppressed by raloxifene. Collectively, these data highlight the crucial role of oestrogen‐induced EMT in the development of adenomyosis and suggest that raloxifene may be a potential therapeutic agent for adenomyosis patients. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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Bulun, S. E. (2009) · New England Journal of Medicine · doi:10.1056/nejmra0804690 · Cited by 1,772
Direct regulation of TWIST by HIF-1α promotes metastasis
Yang, M.-H., Wu, M.-Z., Chiou, S.-H., Chen, P.-M., Chang, S.-Y., Liu, C.-J., Teng, S.-C., & Wu, K.-J. (2008) · Nature Cell Biology · doi:10.1038/ncb1691 · Cited by 1,345
Self-citationZhang, H., Niu, Y., Feng, J., Guo, H., Ye, X., & Cui, H. (2006) · Fertility and Sterility · doi:10.1016/j.fertnstert.2006.01.028 · Cited by 101
Yao, Z., Shen, X., Capodanno, I., Donnelly, M., Fenyk-Melody, J., Hausamann, J., Nunes, C., Strauss, J., & Vakerich, K. (2005) · Journal of Investigative Surgery · doi:10.1080/08941930591004412 · Cited by 60
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Pathogenesis of uterine adenomyosis, invagination or metaplasia?
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Pathogenesis of adenomyosis, an update on molecular mechanisms
Vannuccini, S., Tosti, C., Carmona, F., Huang, S. J., Chapron, C., Guo, S.-W., & Petraglia, F. (2017) · Reproductive BioMedicine Online · doi:10.1016/j.rbmo.2017.06.016 · Cited by 326
Chapron, C., Tosti, C., Marcellin, L., Bourdon, M., Lafay-Pillet, M.-C., Millischer, A.-E., Streuli, I., Borghese, B., Petraglia, F., & Santulli, P. (2017) · Human Reproduction · doi:10.1093/humrep/dex088 · Cited by 294
Adenomyosis: Mechanisms and Pathogenesis
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Metadata
- Authors
- Chen, Y., Li, H., Huang, C., Twu, N., Yen, M., Wang, P., Chou, T., Liu, Y., Chao, K., & Yang, M.
- Venue
- The Journal of Pathology
- Publisher
- Wiley
- Published
- 2010-07-26
- Volume
- 222
- Issue
- 3
- Pages
- 261-270
- ISSN
- 0022-3417 (ISSN-L)
- 1096-9896
- OpenAlex
- W2114428497
- Cited by
- 245
- References
- 4
- FWCI
- 9.11
- Type
- journal article
- Language
- en
- Open access
- bronze
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