ReviewMolecular cancer research : MCR2014
EZH2: not EZHY (easy) to deal.
Review in Molecular cancer research : MCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 2 of them syntheses 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
65 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- The role of EZH2 in overall survival of colorectal cancer: a meta-analysis.Scientific reports · 2017Pooled it
- Patients with chronically diseased livers have lower incidence of colorectal liver metastases: a meta-analysis.PloS one · 2014Pooled it
- Oncogenic Ras drives EED degradation and PRC2 dysfunction to promote aggressive squamous cell carcinoma.Nature communications · 2026Article
- NRF1 predominantly causes EZH2 overexpression in cancer cells.Cell death & disease · 2026Article
- Regulation of androgen receptor expression by enhancer elements in prostate cancer.Experimental & molecular medicine · 2026Review
- Epigenetic Rearrangements Driven by Enhancer of Zeste Homolog 2 Are Linked to Impaired Tissue Regeneration in Neonatal Necrotizing Enterocolitis.Cellular and molecular gastroenterology and hepatology · 2026Article
- Multiple Epigenetic Mechanisms Functionally Cooperate to Silence Expression of Somatostatin Receptor Type 2 in Pancreatic Neuroendocrine Tumors.bioRxiv : the preprint server for biology · 2025Article
- Review
- Exosomal RNAs and EZH2: unraveling the molecular dialogue driving tumor progression.Medical oncology (Northwood, London, England) · 2025Review
- Targeting EZH2 in Cancer: Mechanisms, Pathways, and Therapeutic Potential.Molecules (Basel, Switzerland) · 2024Review
- The potential of EZH2 expression to facilitate treatment choice in stage II colorectal adenocarcinoma.Histology and histopathology · 2024Article
- EZH2: An analysis of a potential new tumor marker in high-risk localization of cutaneous squamous cell carcinomas.Frontiers in oncology · 2024Article
- Dysregulation of iron homeostasis by TfR-1 renders EZH2 wild type diffuse large B-cell lymphoma resistance to EZH2 inhibition.Acta pharmacologica Sinica · 2023Article
- PRC2 disruption in cerebellar progenitors produces cerebellar hypoplasia and aberrant myoid differentiation without blocking medulloblastoma growth.Acta neuropathologica communications · 2023Article
- Exploring the Association Between PRC2 Genes Variants and Lung Cancer Risk in Chinese Han Population.OncoTargets and therapy · 2023Article
- Article
- Transcriptional suppression of Dicer by HOXB-AS3/EZH2 complex dictates sorafenib resistance and cancer stemness.Cancer science · 2022Article
- circNR3C1 Suppresses Bladder Cancer Progression through Acting as an Endogenous Blocker of BRD4/C-myc Complex.Molecular therapy. Nucleic acids · 2020Article
- Clinicopathologic significance of protein lysine methyltransferases in cancer.Clinical epigenetics · 2020Review
- Retrospective analysis on the consistency of MRI features with histological and molecular markers in diffuse intrinsic pontine glioma (DIPG).Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2020Article
5 more citing papers are in PubMed but not listed here.
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.
Funding
Abstract
Seminal discoveries have established that epigenetic modifications are important for driving tumor progression. Polycomb group (PcG) proteins are highly conserved epigenetic effectors that maintain, by posttranslational modification of histones, the silenced state of genes involved in critical biologic processes, including cellular development, stem cell plasticity, and tumor progression. PcG proteins are found in two multimeric protein complexes called Polycomb repressive complexes: PRC1 and PRC2. Enhancer of zeste homolog 2 (EZH2), catalytic core subunit of PRC2, epigenetically silences several tumor-suppressor genes by catalyzing the trimethylation of histone H3 at lysine 27, which serves as a docking site for DNA methyltransferases and histone deacetylases. Evidence suggests that overexpression of EZH2 is strongly associated with cancer progression and poor outcome in disparate cancers, including hematologic and epithelial malignancies. The regulatory circuit and molecular cues causing EZH2 deregulation vary in different cancer types. Therefore, this review provides a comprehensive overview on the oncogenic role of EZH2 during tumorigenesis and highlights the multifaceted role of EZH2, as either a transcriptional activator or repressor depending on the cellular context. Additional insight is provided on the recent understanding of the causes and consequences of EZH2 overexpression in specific cancer types. Finally, evidence is discussed on how EZH2 has emerged as a promising target in anticancer therapy and the prospects for targeting EZH2 without affecting global methylation status. Thus, a better understanding of the complex epigenetic regulatory network controlling EZH2 expression and target genes facilitates the design of novel therapeutic interventions.
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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.