SynthesisOncotarget2014
EZH2 dependent H3K27me3 is involved in epigenetic silencing of ID4 in prostate cancer.
Synthesis in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
What it found
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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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Pooled it
- VprBP drives prostate tumorigenesis by its kinase activity targeting histone H2A.Cell communication and signaling : CCS · 2026Article
- Repurposing acetyldigitoxin as a potential EZH2 inhibitor for non-small cell lung cancer: a computational and experimental approach.Journal of computer-aided molecular design · 2026Article
- Histone-modifying enzymes as drivers and therapeutic targets in androgen-resistant prostate cancer.Frontiers in endocrinology · 2025Review
- ELK3-ID4 axis governs the metastatic features of triple negative breast cancer.Oncology research · 2023Article
- EZH2 modulates retinoic acid signaling to ensure myotube formation during development.FEBS letters · 2022Article
- The Current State of Chromatin Immunoprecipitation (ChIP) from FFPE Tissues.International journal of molecular sciences · 2022Review
- Integrated bioinformatics analysis reveals that EZH2-rich domains promote transcriptional repression in cervical cancer.EXCLI journal · 2022Article
- lncRNA H19 facilitates the proliferation and differentiation of human dental pulp stem cells via EZH2-dependent LATS1 methylation.Molecular therapy. Nucleic acids · 2021Article
- Magic and mystery of microRNA-32.Journal of cellular and molecular medicine · 2021Review
- The Role of H3K4 Trimethylation in CpG Islands Hypermethylation in Cancer.Biomolecules · 2021Review
- Downregulation of histone-lysine N-methyltransferase EZH2 inhibits cell viability and enhances chemosensitivity in lung cancer cells.Oncology letters · 2021Article
- Long noncoding RNA MEG3 blocks telomerase activity in human liver cancer stem cells epigenetically.Stem cell research & therapy · 2020Article
- Article
- Activation of Steroidogenesis, Anti-Apoptotic Activity, and Proliferation in Porcine Granulosa Cells byGenes · 2020Article
- Epigenomic profiling of archived FFPE tissues by enhanced PAT-ChIP (EPAT-ChIP) technology.Clinical epigenetics · 2018Article
- Effects of histone methyltransferase inhibition in endometriosis.Biology of reproduction · 2018Article
- EZH2-mediated suppression of lncRNA-LET promotes cell apoptosis and inhibits the proliferation of post-burn skin fibroblasts.International journal of molecular medicine · 2018Article
- Inhibition of enhancer of zeste homolog 2 increases the expression of p16 and suppresses the proliferation and migration of ovarian carcinoma cellsOncology letters · 2018Article
- EZH2 promotes hepatocellular carcinoma progression through modulating miR-22/galectin-9 axis.Journal of experimental & clinical cancer research : CR · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Inhibitor of DNA binding/differentiation protein 4 (ID4) is dominant negative helix loop helix transcriptional regulator is epigenetically silenced due to promoter hyper-methylation in many cancers including prostate. However, the underlying mechanism involved in epigenetic silencing of ID4 is not known. Here, we demonstrate that ID4 promoter methylation is initiated by EZH2 dependent tri-methylation of histone 3 at lysine 27 (H3K27me3). ID4 expressing (LNCaP) and non-expressing (DU145 and C81) prostate cancer cell lines were used to investigate EZH2, H3K27me3 and DNMT1 enrichment on ID4 promoter by Chromatin immuno-precipitation (ChIP). Enrichment of EZH2, H3K27Me3 and DNMT1 in DU145 and C81 cell lines compared to ID4 expressing LNCaP cell line. Knockdown of EZH2 in DU145 cell line led to re-expression of ID4 and decrease in enrichment of EZH2, H3K27Me3 and DNMT1 demonstrating that ID4 is regulated in an EZH2 dependent manner. ChIP data on prostate cancer tissue specimens and cell lines suggested EZH2 occupancy and H3K27Me3 marks on the ID4 promoter. Collectively, our data indicate a PRC2 dependent mechanism in ID4 promoter silencing in prostate cancer through recruitment of EZH2 and a corresponding increase in H3K27Me3. Increased EZH2 but decreased ID4 expression in prostate cancer strongly supports this model.
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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.