Role of Estrogen Receptor-β in Endometriosis

Bulun, Serdar E.; Monsavais, Diana; Pavone, Mary Ellen; Dyson, Matthew T.; Xue, Qing; Attar, Erkut; Tokunaga, Hideki; Su, Emily J.

doi:10.1055/s-0031-1299596

Cited by 254 publications

(203 citation statements)

References 65 publications

(69 reference statements)

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“…Estrogen and progesterone exert their biological functions through binding to their specific receptors in the endometrium, and the expression levels of these receptors are periodically changed in accordance with the normal menstrual cycle of healthy women (Bulun et al, 2012;Henriet et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Effects of icariin on the expression of ER, VEGF, and KDR in the endometrial cells of thin endometrium

Le¹,

Shan²,

Wang³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. We explored the effects of icariin on the expression of estrogen receptor (ER), vascular endothelial growth factor (VEGF), and kinase insert domain receptor (KDR) in the endometrial cells of the thin endometrium. Primary endometrial cells were obtained and divided into a blank control group, a high-, a middle-, and a low-dose icariin groups, as well as an estrogen treatment group to undergo cellular identification by immunocytochemistry. The expression levels of ER, VEGF, and its receptor were estimated by western blotting. The expression levels of ER, VEGF, and KDR gradually increased from the control group to the estrogen (E2) treatment and icariin treatment groups; the differences were statistically significant. However, the differences were not statistically significant among the different icariin dose groups. The endometrium may be thickened by icariin treatment by increasing the expression levels of ER, VEGF, and KDR in endometrial cells.

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Section: Discussionmentioning

confidence: 99%

Effects of icariin on the expression of ER, VEGF, and KDR in the endometrial cells of thin endometrium

Le¹,

Shan²,

Wang³

et al. 2015

Genet. Mol. Res.

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“…Dysregulated E2 metabolism has been reported to contribute to a variety of human diseases including leiomyoma, endometriosis, osteoporosis, Parkinson disease, and gynecological malignancies (31)(32)(33)(34)(35). Recently, Flamini et al (36) reported that E2 could regulate endometrial cell cytoskeletal remodeling and motility via focal adhesion kinase.…”

Section: Anxa2 Knockdown Compromises Growth Metastasis and Proangiomentioning

confidence: 99%

Proteomics Identification of Annexin A2 as a Key Mediator in the Metastasis and Proangiogenesis of Endometrial Cells in Human Adenomyosis

Zhou

et al. 2012

Molecular & Cellular Proteomics

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Adenomyosis is a common estrogen-dependent disorder of females characterized by a downward extension of the endometrium into the uterine myometrium and neovascularization in ectopic lesions. It accounts for chronic pelvic pain, dysmenorrhea, menorrhagia, and infertility in 8.8 -61.5% women worldwide. However, the molecular mechanisms for adenomyosis development remain poorly elucidated. Here, we utilized a two-dimensional polyacrylamide gel electrophoresis/MS-based proteomics analysis to compare and identify differentially expressed proteins in matched ectopic and eutopic endometrium of adenomyosis patients. A total of 93 significantly altered proteins were identified by tandem MS analysis. Further cluster analysis revealed a group of estrogen-responsive proteins as dysregulated in adenomyosis, among which annexin A2, a member of annexin family proteins, was found up-regulated most significantly in the ectopic endometrium of adenomyosis compared with its eutopic counterpart. Overexpression of ANXA2 was validated in ectopic lesions of human adenomyosis and was found to be tightly correlated with markers of epithelial to mesenchymal transition and dysmenorrhea severity of adenomyosis patients. Functional analysis demonstrated that estrogen could remarkably up-regulate ANXA2 and induce epithelial to mesenchymal transition in an in vitro adenomyosis model. Enforced expression of ANXA2 could mediate phenotypic mesenchymal-like cellular changes, with structural and functional alterations in a ␤-catenin/T-cell factor (Tcf) signaling-associated manner, which could be reversed by inhibition of ANXA2 expression. We also proved that enforced expression of ANXA2 enhanced the proangiogenic capacity of adenomyotic endometrial cells through HIF-1␣/VEGF-A pathway. In vivo, we demonstrated that ANXA2 inhibition abrogated endometrial tissue growth, metastasis, and angiogenesis in an adenomyosis nude mice model and significantly alleviated hyperalgesia. Taken together, our data unraveled a dual role for ANXA2 in the pathogenesis of human adenomyosis through conferring endometrial cells both metastatic potential and proangiogenic capacity, which could serve as a potential therapeutic target for the treatment of adenomyosis patients.

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“…PGE2, as well as the EGF, upregulate aromatase (CYP19) expression, the enzyme that plays a key role in estrogen (E2) biosynthesis (20)(21). The biologically active E2 aggravates pathologic processes including inflammation and influences the risk of cancer through an inflammation-related mechanism (22)(23)(24). Lately, the aromatase (CYP19A1) has been identified in malignant mesothelioma (25).…”

Section: Malignant Mesothelioma Molecular Targets Involved In Inflammmentioning

confidence: 99%

Cyclooxygenase-2, Epidermal Growth Factor Receptor, and Aromatase Signaling in Inflammation and Mesothelioma

Nuvoli¹,

Galati²

2013

Molecular Cancer Therapeutics

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Malignant mesothelioma or mesothelioma is a rare form of cancer that develops from transformed cells originating in the mesothelium, the protective lining that covers many of the internal organs of the body. It is directly linked to asbestos exposure, which acts as a carcinogen by initiating the carcinogenic process. Because of their shape, asbestos fibers can cross the membrane barriers inside the body and cause inflammatory and fibrotic reactions. Such reactions are believed to be the mechanism by which asbestos fibers may trigger malignant mesothelioma in the pleural membrane around the lungs. Carcinogens are known to modulate the transcription factors, antiapoptotic proteins, proapoptotic proteins, protein kinases, cell-cycle proteins, cell adhesion molecules, COX-2, and growth factor signaling pathways. This article reviews recent studies regarding some malignant mesothelioma molecular targets not only for cancer prevention but also for cancer therapy.

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Role of Estrogen Receptor-β in Endometriosis

Cited by 254 publications

References 65 publications

Effects of icariin on the expression of ER, VEGF, and KDR in the endometrial cells of thin endometrium

Effects of icariin on the expression of ER, VEGF, and KDR in the endometrial cells of thin endometrium

Proteomics Identification of Annexin A2 as a Key Mediator in the Metastasis and Proangiogenesis of Endometrial Cells in Human Adenomyosis

Cyclooxygenase-2, Epidermal Growth Factor Receptor, and Aromatase Signaling in Inflammation and Mesothelioma

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