ArticleMolecular cancer2023
EZH2 mediated metabolic rewiring promotes tumor growth independently of histone methyltransferase activity in ovarian cancer.
Article in Molecular cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 58 citations in OpenAlex.
- Structural characteristics and SARs of EZH2 inhibitors.Molecular diversity · 2026Review
- Epigenetic and chromatin remodeling mechanisms across cardiomyopathies: a comprehensive review.Epigenetics & chromatin · 2026Review
- Identification and validation of an m1A-score model to predict outcomes and immunomodulation in lung squamous cell carcinoma by integrated analysis of single-cell and bulk RNA sequencing.Discover oncology · 2026Article
- Combined Assessment of EZH2 and EGFR as Potential Diagnostic Biomarkers for Epithelial Ovarian Tumors: Bioinformatics Analysis and Clinical Validation.International journal of women's health · 2026Article
- EZH2 blockade reverses doxorubicin resistance by inducing metabolic vulnerability and enhancing DNA damage in breast cancer.Frontiers in pharmacology · 2026Article
- The Role of COQ10B in Tumor Progression and Its Association with Immune Escape in Esophageal Squamous Cell Carcinoma: A Multi-Omics and Functional Analysis.International journal of general medicine · 2026Article
- Anti-tumor effects and mechanism of the histone demethylase inhibitor GSK-J4 in non-small cell lung cancer cells.Medical oncology (Northwood, London, England) · 2025Article
- RNA sequencing in ovarian cancer research: a comprehensive review.Journal of ovarian research · 2025Review
- Therapeutic targeting of post-translational modifications in ovarian cancer: mechanisms and clinical applications.Journal of ovarian research · 2025Review
- Trained Immunity in Health and Disease.MedComm · 2025Review
- Understanding and overcoming multidrug resistance in cancer.Nature reviews. Clinical oncology · 2025Review
- Review
- Ginsenoside 20(S)-Rg3 upregulates SQLE to reprogram cholesterol metabolism of ovarian cancer cells.iScience · 2025Article
- A novel effect of sulforaphane on promoting mouse granulosa cells proliferation via the NRF2-TKT pathway.Journal of advanced research · 2025Article
- Article
- Branched-chain amino acid and cancer: metabolism, immune microenvironment and therapeutic targets.Journal of translational medicine · 2025Review
- EZH2,World journal of stem cells · 2025Article
- Bridging epigenomics and tumor immunometabolism: molecular mechanisms and therapeutic implications.Molecular cancer · 2025Review
- Aging and tumors: a dynamic interaction.Discover oncology · 2025Review
- Organoid models of ovarian cancer: resolving immune mechanisms of metabolic reprogramming and drug resistance.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
21 authors at 10 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEnhancer of zeste homolog 2 (EZH2), the key catalytic subunit of polycomb repressive complex 2 (PRC2), is overexpressed and plays an oncogenic role in various cancers through catalysis-dependent or catalysis-independent pathways. However, the related mechanisms contributing to ovarian cancer (OC) are not well understood.
methodsThe levels of EZH2 and H3K27me3 were evaluated in 105 OC patients by immunohistochemistry (IHC) staining, and these patients were stratified based on these levels. Canonical and noncanonical binding sites of EZH2 were defined by chromatin immunoprecipitation sequencing (ChIP-Seq). The EZH2 solo targets were obtained by integrative analysis of ChIP-Seq and RNA sequencing data. In vitro and in vivo experiments were performed to determine the role of EZH2 in OC growth.
resultsWe showed that a subgroup of OC patients with high EZH2 expression but low H3K27me3 exhibited the worst prognosis, with limited therapeutic options. We demonstrated that induction of EZH2 degradation but not catalytic inhibition profoundly blocked OC cell proliferation and tumorigenicity in vitro and in vivo. Integrative analysis of genome-wide chromatin and transcriptome profiles revealed extensive EZH2 occupancy not only at genomic loci marked by H3K27me3 but also at promoters independent of PRC2, indicating a noncanonical role of EZH2 in OC. Mechanistically, EZH2 transcriptionally upregulated IDH2 to potentiate metabolic rewiring by enhancing tricarboxylic acid cycle (TCA cycle) activity, which contributed to the growth of OC.
conclusionsThese data reveal a novel oncogenic role of EZH2 in OC and identify potential therapeutic strategies for OC by targeting the noncatalytic activity of EZH2.
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