ReviewCancers2025
EZH2 Dysregulation and Its Oncogenic Role in Human Cancers.
Review in Cancers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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
15 citing papers in PubMed.
- Epigenetic Plasticity in Triple-Negative Breast Cancer: Mechanisms of Therapy Resistance, Biomarkers, and Therapeutic Vulnerabilities.Biomedicines · 2026Review
- The Role of IGF2BP3-Mediated Immune Response Activation in Enhancing Immunotherapy of Koumine for Gastric Cancer.Cancer science · 2026Article
- Stage-dependent expression and nuclear localization of EZH2 in endometrial carcinogenesis: evidence from cell lines and human tissues.Journal of molecular histology · 2026Article
- EZH2 Regulates the Proliferation-Senescence Balance and Tumor-Stromal Signaling in Lung Adenocarcinoma.International journal of molecular sciences · 2026Article
- An integrated multi-omics analysis reveals a core epigenetically-activated transcriptional network driving oncogenic signaling in acute myeloid leukemia.Discover oncology · 2026Article
- Transcriptomic Evidence of Immune-Tumor Uncoupling Defines a High-Risk State in Uterine Corpus Endometrial Carcinoma.International journal of molecular sciences · 2026Article
- SOX-2 and EZH-2 Expression in Primary Epithelial Malignant Salivary Gland Tumors.Medical sciences (Basel, Switzerland) · 2026Article
- Co-Occurrence of Nuclear-Catenin and H3K27me3 Expression in Advanced Colorectal Cancer: A Retrospective Observational Study.Current oncology (Toronto, Ont.) · 2026Observational
- Molecular Mechanisms in Oral Squamous Cell Carcinoma: Integrative Roles of Cancer-Associated Fibroblasts, Immune Microenvironment, and Precision Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Review
- Molecular and Immune Mechanisms Governing Cancer Metastasis, Including Dormancy, Microenvironmental Niches, and Tumor-Specific Programs.International journal of molecular sciences · 2026Review
- EZH2 in Acral Lentiginous Melanoma: Molecular, Epigenetic, and Therapeutic Perspectives.Oncology research · 2026Review
- Genomic innovations in cancer prevention, diagnosis, prognosis and precision therapeutics.Frontiers in genetics · 2026Review
- Molecular reprogramming in cutaneous melanoma: the central role of G9a and EZH2 methyltransferase inhibitors in tumor plasticity, immune evasion, and therapeutic resistance.Frontiers in pharmacology · 2026Review
- Epigenomic and Metabolic Interplay in the Development of Metastatic Brain Tumors.Oncology research · 2026Review
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.
Funding
Abstract
Enhancer of Zeste Homolog 2 (EZH2) is a key epigenetic regulator known for its role in global gene silencing and is involved in a variety of cellular processes, including cell survival, proliferation, invasion, and self-renewal. As a core component of the Polycomb Repressive Complex 2 (PRC2), EZH2 catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3), leading to chromatin compaction and transcriptional repression. Dysregulated EZH2 expression is observed in a wide range of solid tumors and hematological malignancies and is frequently associated with increased metastatic potential and poor clinical outcomes. While EZH2 primarily mediates gene silencing through its canonical PRC2-dependent activity, it also exerts oncogenic effects via non-canonical mechanisms. In its non-canonical role, EZH2 acts independently of PRC2, interacting with other signaling molecules as a transcriptional activator or co-activator, thereby promoting the activation of oncogenic pathways. Through both canonical and non-canonical mechanisms, EZH2 significantly contributes to tumor initiation and its subsequent progression. Given its critical role in oncogenesis and cancer progression, EZH2 is under investigation as a potential biomarker for cancer diagnosis and prognosis. This review provides a comprehensive overview of EZH2's function and oncogenic roles across human cancers. Enhanced insight into EZH2's complex regulatory network may facilitate the development of more effective strategies to manage EZH2-driven malignancies.
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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.