ArticleMolecular endocrinology (Baltimore, Md.)2014
ERβ- and prostaglandin E2-regulated pathways integrate cell proliferation via Ras-like and estrogen-regulated growth inhibitor in endometriosis.
Article in Molecular endocrinology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Chronic Endometritis and Endometriosis: Two Sides of the Same Coin?Reproductive sciences (Thousand Oaks, Calif.) · 2025Pooled it
- Comprehensive transcript and protein profiling reveals ERα rather than ERβ as the predominant estrogen receptor in human endometriotic lesions.Communications biology · 2026Article
- Hormonal Dysregulation and Neuroinflammation in Endometriosis: Convergent Druggable Pathways.Current issues in molecular biology · 2026Review
- Cancer-like Hallmarks of Endometriosis: The Role of Estrogen Signaling and Stem Cell Plasticity.International journal of molecular sciences · 2026Review
- Autophagy and Lysosomal Dysregulation in Endometriosis: Therapeutic Opportunities and Molecular Insights.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Whole-body RNA Sequencing Analysis of the Post-larval Reveals the Sex-biased Gene and MiRNA in the Prawn Macrobrachium rosenbergii.Marine biotechnology (New York, N.Y.) · 2026Article
- Genetically predicted triglyceride levels and endometriosis risk: Mendelian randomization with exploratory multi-omics analyses.PloS one · 2026Article
- Endometrial Stromal Cells from Endometriosis Patients Reflect Lesion-Type-Specific Heterogeneity.Cells · 2025Article
- Epigenetic regulation of nuclear receptors: Implications for endocrine-related diseases and therapeutic strategies.Genes & diseases · 2025Review
- Prospects for potential therapy targeting immune‑associated factors in endometriosis (Review).Molecular medicine reports · 2025Review
- Endometriotic lesions exhibit distinct metabolic signature compared to paired eutopic endometrium at the single-cell level.Communications biology · 2024Article
- N-Myc and STAT Interactor is an Endometriosis Suppressor.International journal of molecular sciences · 2024Article
- Immune pathway through endometriosis to ovarian cancer.World journal of clinical oncology · 2024Review
- Article
- The Cellular Respiration of Endometrial Biopsies from Patients with Various Forms of Endometriosis.International journal of molecular sciences · 2024Article
- The mysterious association between adiponectin and endometriosis.Frontiers in pharmacology · 2024Review
- Relationship between Cardiometabolic index and endometriosis in a US nationally representative sample: results from NHANES 1999-2006.Frontiers in endocrinology · 2024Article
- Article
- Genetic analysis confirms a link between gastrointestinal disorders and endometriosis.Cell reports. Medicine · 2023Article
- Evidence of shared genetic factors in the etiology of gastrointestinal disorders and endometriosis and clinical implications for disease management.Cell reports. Medicine · 2023Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
In endometriosis, stromal and epithelial cells from the endometrium form extrauterine lesions and persist in response to estrogen (E2) and prostaglandin E2 (PGE2). Stromal cells produce excessive quantities of estrogen and PGE2 in a feed-forward manner. However, it is unknown how estrogen stimulates cell proliferation and survival for the establishment and persistence of disease. Previous studies suggest that estrogen receptor-β (ERβ) is strikingly overexpressed in endometriotic stromal cells. Thus, we integrated genome-wide ERβ binding data from previously published studies in breast cells and gene expression profiles in human endometriosis and endometrial tissues (total sample number = 81) and identified Ras-like, estrogen-regulated, growth inhibitor (RERG) as an ERβ target. Estradiol potently induced RERG mRNA and protein levels in primary endometriotic stromal cells. Chromatin immunoprecipitation demonstrated E2-induced enrichment of ERβ at the RERG promoter region. PGE2 via protein kinase A phosphorylated RERG and enhanced the nuclear translocation of RERG. RERG induced the proliferation of primary endometriotic cells. Overall, we demonstrated that E2/ERβ and PGE2 integrate at RERG, leading to increased endometriotic cell proliferation and represents a novel candidate for therapeutic intervention.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.