Genomic Function of Estrogen Receptor β in Endometriosis

Han, Sang Jun; Lee, Jiyeun E; Cho, Yeon Jean; Park, Mi Jin; O’Malley, Bert W.

doi:10.1210/en.2019-00442

Cited by 47 publications

(39 citation statements)

References 77 publications

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“…Previous studies have reported ERβ chromatin binding in other types of cells, including breast cancer cell lines, 32,36,54,69,70 rat germ cells, 71 endometriosis, 72 and in U20S cells. 73 However, most ERβ antibodies are not specific towards ERβ protein 33,34 and our study is the first to use the validated PPZ0506 antibody in ChIP-Seq.…”

Section: Discussionmentioning

confidence: 99%

Genome‐wide estrogen receptor β chromatin binding in human colon cancer cells reveals its tumor suppressor activity

Indukuri

Jafferali

Song

et al. 2021

Intl Journal of Cancer

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Colorectal cancer (CRC) is the third leading cause of cancer death in the western world.In women, menopausal hormone therapy has been shown to reduce CRC incidence by 20%. Studies demonstrate that estrogen activating estrogen receptor beta (ERβ) protects against CRC. ERβ is a nuclear receptor that regulates gene expression through interactions with the chromatin. This molecular mechanism is, however, not well characterized in colon. Here, we present for the first time, the cistrome of ERβ in different colon cancer cell lines. We use cell lines engineered to express ERβ, optimize and validate an ERβ antibody for chromatin-immunoprecipitation (ChIP), and perform ChIP-Seq.We identify key binding motifs, including ERE, AP-1, and TCF sites, and we determine enrichment of binding to cis-regulatory chromatin sites of genes involved in tumor development, cell migration, cell adhesion, apoptosis, and Wnt signaling pathways. We compare the corresponding cistromes of colon and breast cancer and find that they are conserved for about a third of genes, including GREB1, but that ERβ tethering to TCF and KLF family motifs is characteristic for colon. We exemplify upregulation of putative CRC tumor suppressor gene CST5 where ERβ in colon cells binds to cis-regulatory regions nearby (−351 bp) the transcriptional start site. Our work provides a foundation for understanding the mechanism of action of ERβ in CRC prevention.

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Section: Discussionmentioning

confidence: 99%

Genome‐wide estrogen receptor β chromatin binding in human colon cancer cells reveals its tumor suppressor activity

Indukuri

Jafferali

Song

et al. 2021

Intl Journal of Cancer

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“…At the cytoplasmatic level, ER β was reported involved in the inhibition and disruption of TNF- α -induced apoptosis signaling [88]. At nuclear level, ER β was identified involved in the direct activation of the NFkB pathway and the radical oxygen species detoxification system, that are able to improve cell survival and cell escaping from immune clearance [92]. At the same time, ER β was related to the upregulation of hypoxia-induced signaling, epithelial mesenchymal transition signaling, and cytoskeleton components, that are all involved in the invasion and progression of endometriotic implants [92].…”

Section: Behind the Origins Of Endometriosismentioning

confidence: 99%

The Pathogenesis of Endometriosis: Molecular and Cell Biology Insights

Laganà

Garzon

Götte

et al. 2019

IJMS

356

265

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The etiopathogenesis of endometriosis is a multifactorial process resulting in a heterogeneous disease. Considering that endometriosis etiology and pathogenesis are still far from being fully elucidated, the current review aims to offer a comprehensive summary of the available evidence. We performed a narrative review synthesizing the findings of the English literature retrieved from computerized databases from inception to June 2019, using the Medical Subject Headings (MeSH) unique ID term “Endometriosis” (ID:D004715) with “Etiology” (ID:Q000209), “Immunology” (ID:Q000276), “Genetics” (ID:D005823) and “Epigenesis, Genetic” (ID:D044127). Endometriosis may origin from Müllerian or non-Müllerian stem cells including those from the endometrial basal layer, Müllerian remnants, bone marrow, or the peritoneum. The innate ability of endometrial stem cells to regenerate cyclically seems to play a key role, as well as the dysregulated hormonal pathways. The presence of such cells in the peritoneal cavity and what leads to the development of endometriosis is a complex process with a large number of interconnected factors, potentially both inherited and acquired. Genetic predisposition is complex and related to the combined action of several genes with limited influence. The epigenetic mechanisms control many of the processes involved in the immunologic, immunohistochemical, histological, and biological aberrations that characterize the eutopic and ectopic endometrium in affected patients. However, what triggers such alterations is not clear and may be both genetically and epigenetically inherited, or it may be acquired by the particular combination of several elements such as the persistent peritoneal menstrual reflux as well as exogenous factors. The heterogeneity of endometriosis and the different contexts in which it develops suggest that a single etiopathogenetic model is not sufficient to explain its complex pathobiology.

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“…NF-κB has been reported to be overexpressed in endometriosis, including ectopic lesions, the eutopic endometrium, endometriotic stromal cells, and peritoneal macrophages [15]. Estrogen plays an important role in endometriosis, and there are cell-type-specific interactions between estrogen receptors (ERs) and NF-κB signaling [30]. ERs block the binding of DNA to NF-κB in endometrial stromal cells.…”

Section: Discussionmentioning

confidence: 99%

Overexpressed MPS-1 contributes to endometrioma development through the NF-κB signaling pathway

Liu

Zhang

et al. 2021

Reprod Biol Endocrinol

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Background Endometriosis is a benign gynecological disease that shares some characteristics with malignant tumors and affects approximately 10% of women of reproductive age. Endometrioma refers to endometriosis that appears in the ovary. Metallopanstimulin-1 (MPS-1) is a component of the 40S subunit of ribosomes that has extra-ribosomal functions that contribute to the development of diseases. This study aimed to explore the expression pattern and role of MPS-1 in endometrioma development. Methods Quantitative real time polymerase chain reaction, western blotting, immunohistochemistry, and enzyme-linked immunosorbent assay were used to determine the expression of MPS-1 in patients with endometrioma. Following the successful knockdown of MPS-1 by siRNA, CCK-8 assays, flow cytometry, and transwell assays were performed to detect ectopic endometrial stromal cells (EcESCs) proliferation, the rate of apoptosis, and cell cycle, migration, and invasion, respectively. Western blotting was used to explore the effect of MPS-1 knockdown on protein levels in the NF-κB signaling pathway. Results The expression of MPS-1 was significantly higher in endometrioma and the serum of endometrioma patients than in the patients without endometriosis. In addition, the downregulation of MPS-1 expression inhibited EcESCs proliferation, migration, and invasion. This downregulation led to the arrest of the EcESCs cycle in the G0/G1 phase and apoptosis and depressed the NF-κB signaling pathway. Conclusion MPS-1 can regulate EcESCs proliferation, motility, invasion, apoptosis, and cell cycle via the NF-κB signaling pathway in endometrioma. This may contribute to the formation or development of endometriotic foci. This study suggests the potential role of MPS-1 in the pathogenesis of endometriosis and enabled further research into the use of MPS-1 in the clinical diagnosis of endometrioma.

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Genomic Function of Estrogen Receptor β in Endometriosis

Cited by 47 publications

References 77 publications

Genome‐wide estrogen receptor β chromatin binding in human colon cancer cells reveals its tumor suppressor activity

Genome‐wide estrogen receptor β chromatin binding in human colon cancer cells reveals its tumor suppressor activity

The Pathogenesis of Endometriosis: Molecular and Cell Biology Insights

Overexpressed MPS-1 contributes to endometrioma development through the NF-κB signaling pathway

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