ArticleScientific reports2017
Enhancer of Zeste homolog 2 (EZH2) induces epithelial-mesenchymal transition in endometriosis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- The role of fibrosis in endometriosis: a systematic review.Human reproduction update · 2024Pooled it
- Metabolic remodeling of endometriosis microenvironment: Energy stress and immune evasion.iScience · 2026Review
- Epigenetics, Oxidative Stress, and the Microbiome in Endometriosis: Toward an Integrated Mechanistic Framework for Precision Medicine.Journal of personalized medicine · 2026Review
- Cancer-like Hallmarks of Endometriosis: The Role of Estrogen Signaling and Stem Cell Plasticity.International journal of molecular sciences · 2026Review
- Unravelling the molecular crosstalk between Epithelial-Mesenchymal transition and human papillomavirus in oral cancer.Molecular biology reports · 2025Review
- H3K27me3-mediated epigenetic regulation of TET1 in the eutopic endometrium of women with endometriosis and infertility.Scientific reports · 2025Article
- Unraveling the interrelationship between breast cancer and endometriosis based on multi-omics analysis.Discover oncology · 2025Article
- Dual targeting of CXCR4 and EZH2 in endometriosis.iScience · 2025Article
- Molecular Basis of Impaired Decidualization in the Eutopic Endometrium of Endometriosis Patients.Cells · 2025Review
- EZH2 promotes endometriosis progression through estrogen receptor and TNFα expression.Frontiers in endocrinology · 2025Article
- The long road of drug development for endometriosis - Pains, gains, and hopes.Journal of controlled release : official journal of the Controlled Release Society · 2024Review
- Article
- Exploring the Shared Pathogenesis Mechanisms of Endometriosis and Cancer: Stemness and Targeted Treatments of Its Molecular Pathways-A Narrative Review.International journal of molecular sciences · 2024Review
- The involvement of RNA N6-methyladenosine and histone methylation modification in decidualization and endometriosis-associated infertility.Clinical and translational medicine · 2024Article
- Regulation of EZH2 Expression by INPP4B in Normal Prostate and Primary Prostate Cancer.Cancers · 2023Article
- Epigenetic Dysregulation in Endometriosis: Implications for Pathophysiology and Therapeutics.Endocrine reviews · 2023Review
- Endometriosis Stem Cells as a Possible Main Target for Carcinogenesis of Endometriosis-Associated Ovarian Cancer (EAOC).Cancers · 2022Review
- Role of EZH2 in Uterine Gland Development.International journal of molecular sciences · 2022Article
- EZH2 regulates oncomiR-200c and EMT markers in esophageal squamous cell carcinomas.Scientific reports · 2022Article
- Downregulation of EZH2 in Trophoblasts Induces Decidual M1 Macrophage Polarization: a Potential Cause of Recurrent Spontaneous Abortion.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
EZH2, a subunit of the polycomb repressive complex 2 (PRC2) catalyzing trimethylation of histone H3 lysine 27 (H3K27), induces epithelial-mesenchymal transition (EMT) in cancers. However, whether EZH2 regulates EMT in endometriosis is unclear. Here, we show that EZH2 expression, along with its associated PRC2 proteins, is significantly elevated in ectopic and eutopic endometrium from women with endometriosis as compared with control endometrium. EZH2 knockdown or inhibition restored the epithelial phenotypes of endometriotic epithelial cells, concomitant with the upregulation of E-cadherin and downregulation of vimentin and transcription factors (Snail and Slug) as well as reduced cellular migratory and invasive propensity. Conversely, overexpression of EZH2 induced the expression of Snail, Slug and vimentin and suppresses E-cadherin expression. In vivo administration of 3-Deazaneplanocin A (DZNep), an EZH2 inhibitor, significantly inhibited the growth of endometriotic lesions and improved generalized hyperalgesia, along with attenuated EMT and reduced fibrosis in endometriosis. Notably, platelets induced EZH2 upregulation and increased H3K27 and H3K9 trimethylation levels in endometriotic epithelial cells. These data identify EZH2 as a novel driver of EMT in endometriosis, implicates the link between wound healing and epigenetic changes in the context of endometriosis, and underscore the role of platelets in the development of endometriosis.
Indexed as
Identifiers
What OpenQuestion holds
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.