Prolonged stimulation with tumor necrosis factor-alpha induced partial methylation at PR-B promoter in immortalized epithelial-like endometriotic cells
Lab / animal
OA: closed
CC0
⤵ 50 in-corpus citations
AI-generated summary
Tumor necrosis factor-α prolonged stimulation induced partial methylation at the PR-B promoter in immortalized epithelial-like endometriotic cells.
One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works
Abstract
The promoter of P receptor isoform B (PR-B) has recently been shown to be hypermethylated in endometriotic tissues, but one question remains as what causes the aberrant methylation. We show that sustained stimulation of an epithelial-like endometriotic cell line with tumor necrosis factor alpha stimulation for 30 days induced partial methylation in the promoter region of PR-B with concomitant reduction of PR-B expression.
My notes (saved in your browser only)
Condition tags
MeSH descriptors
Citation neighborhood (2-hop)
Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]
References (30)
- Aberrant expression of deoxyribonucleic acid methyltransferases DNMT1, DNMT3A, and DNMT3B in women with endometriosis via openalex
- Identification of an invasive, N-cadherin-expressing epithelial cell type in endometriosis using a new cell culture model via openalex
- Immunobiology of endometriosis via openalex
- Inhibition of proliferation of endometrial stromal cells by trichostatin A, RU486, CDB-2914, N-acetylcysteine, and ICI 182780 via openalex
- Is endometriosis associated with systemic subclinical inflammation? via openalex
- Nuclear factor-kappab (NF-kappaB): an unsuspected major culprit in the pathogenesis of endometriosis that is still at large? via openalex
- Promoter hypermethylation of progesterone receptor isoform B (PR-B) in endometriosis via openalex
- Reduced progesterone action during endometrial maturation: a potential risk factor for the development of endometriosis via openalex
- Role of cytokines in endometriosis via openalex
- The estrogen early response gene FOS is altered in a baboon model of endometriosis via openalex
- The role of cytokines in endometriosis via openalex
- W2122066579 via openalex
- W2122994808 via openalex
- W2143762235 via openalex
- W2162764250 via openalex
- W2324384090 via openalex
- W4211081176 via openalex
- W6678029821 via openalex
- W6678483006 via openalex
- W6681302908 via openalex
- W1994465394 via openalex
- W2001963326 via openalex
- W2013050589 via openalex
- W2030069314 via openalex
- W2031089158 via openalex
- W2040257851 via openalex
- W2059479474 via openalex
- W2065643273 via openalex
- W2109801386 via openalex
- W2121585544 via openalex
Cited by (50)
- Hormonal Dysregulation and Neuroinflammation in Endometriosis: Convergent Druggable Pathways 2026
- Results of dienogest treatment and its discontinuation in patients with symptomatic adenomyosis: a prospective cohort study 2025
- Epigenetics of endometriosis 2025
- Immunologic Aspects of Endometriosis 2024
- Non-response to first-line hormonal treatment for symptomatic endometriosis: overcoming tunnel vision. A narrative review 2023
- From Retrograde Menstruation to Endometrial Determinism and a Brave New World of "Root Treatment" of Endometriosis: Destiny or a Fanciful Utopia? 2023
- Distinct subtypes of endometriosis identified based on stromal-immune microenvironment and gene expression: implications for hormone therapy 2023
- Progesterone Resistance in Endometriosis: Current Evidence and Putative Mechanisms 2023
- Epigenetics, endometriosis and sex steroid receptors: An update on the epigenetic regulatory mechanisms of estrogen and progesterone receptors in patients with endometriosis 2023
- Cracking the enigma of adenomyosis: an update on its pathogenesis and pathophysiology 2022
- Progesterone receptor ligands for the treatment of endometriosis 2022
- Progesterone Actions and Resistance in Gynecological Disorders 2022
- Epithelial-to-mesenchymal transition contributes to the downregulation of progesterone receptor expression in endometriosis lesions 2021
- Three-Dimensional Biofabrication Models of Endometriosis and the Endometriotic Microenvironment 2020
- Epigenetics of Estrogen and Progesterone Receptors in Endometriosis 2020
- Progesterone receptor ligands for the treatment of endometriosis: the mechanisms behind therapeutic success and failure 2020
- Impaired pathogen-induced autophagy and increased IL-1β and TNFα release in response to pathogenic triggers in secretory phase endometrial stromal cells of endometriosis patients 2020
- Three-Dimensional Biofabrication Models of Endometriosis and the Endometriotic Microenvironment 2020
- Endometriosis and nuclear receptors 2019
- Cancer-associated mutations in endometriosis: shedding light on the pathogenesis and pathophysiology 2019
- Endometriosis and Epigenetics: What do we Know? 2018
- Progesterone Resistance in Endometriosis: an Acquired Property? 2018
- Epigenetics of Endometriosis 2018
- Progesterone resistance in endometriosis: origins, consequences and interventions 2017
- Epigenetic regulation of the pathological process in endometriosis 2017
- Progesterone Alleviates Endometriosis via Inhibition of Uterine Cell Proliferation, Inflammation and Angiogenesis in an Immunocompetent Mouse Model 2016
- Innovations in classical hormonal targets for endometriosis 2015
- Selective inhibition of prostaglandin E2 receptors EP2 and EP4 modulates DNA methylation and histone modification machinery proteins in human endometriotic cells 2015
- Association between DNMT3L polymorphic variants and the risk of endometriosis-associated infertility 2015
- Endometriosis and possible inflammation markers 2015
- Epigenetics in Endometriosis 2014
- Influence of AKT on progesterone action in endometrial diseases 2014
- Potential New Drugs for Endometriosis: Experimental Evidence 2014
- Epigenetic background of the most common non-oncologic gynecological diseases 2014
- Decreased expression of mucin-1 in endometriosis endometrium correlated with progesterone receptor B involved in infertility 2014
- Epigenetic aberration of gene expression in endometriosis 2013
- Medical management of endometriosis: emerging evidence linking inflammation to disease pathophysiology 2013
- Western herbal medicine, epigenetics, and endometriosis 2013
- Valproic acid and progestin inhibit lesion growth and reduce hyperalgesia in experimentally induced endometriosis in rats 2012
- The Epigenetics of Endometriosis 2012
- Genetic polymorphisms of DNMT3L involved in hypermethylation of chromosomal ends are associated with greater risk of developing ovarian endometriosis 2012
- Aberrant DNA methylation status of endometriosis: epigenetics as the pathogenesis, biomarker and therapeutic target 2011
- Application of the histone deacetylase inhibitors for the treatment of endometriosis: histone modifications as pathogenesis and novel therapeutic target 2011
- Research resource: genome-wide profiling of methylated promoters in endometriosis reveals a subtelomeric location of hypermethylation 2010
- Constitutive and tumor necrosis factor-alpha-stimulated activation of nuclear factor-kappaB in immortalized endometriotic cells and their suppression by trichostatin A 2010
- Selective inhibition of prostaglandin E2 receptors EP2 and EP4 induces apoptosis of human endometriotic cells through suppression of ERK1/2, AKT, NFkappaB, and beta-catenin pathways and activation of intrinsic apoptotic mechanisms 2009
- Selective Inhibition of Prostaglandin E2 Receptors EP2 and EP4 Induces Apoptosis of Human Endometriotic Cells through Suppression of ERK1/2, AKT, NFκB and β-CATENIN Pathways and Activation of Intrinsic Apoptotic Mechanisms 2009
- Emerging drugs for endometriosis 2008
- Induction of peritoneal endometriosis in nude mice with use of human immortalized endometriosis epithelial and stromal cells: a potential experimental tool to study molecular pathogenesis of endometriosis in humans 2008
- The knockdown of progesterone receptor isoform B (PR-B) promotes proliferation in immortalized endometrial stromal cells 2008
Source provenance
- europepmc
- last seen: 2026-10-11T09:27:45.537177+00:00
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
- pubmed
- last seen: 2026-10-08T21:04:39.942088+00:00
- unpaywall
- last seen: 2026-09-17T06:32:46.214484+00:00
License: CC0
· commercial use OK