ArticleCancer discovery2016
Oncogenic Deregulation of EZH2 as an Opportunity for Targeted Therapy in Lung Cancer.
Article in Cancer discovery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
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Who cites it
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.
- Systematic literature review reveals suboptimal use of chemical probes in cell-based biomedical research.Nature communications · 2023Pooled it
- Structural characteristics and SARs of EZH2 inhibitors.Molecular diversity · 2026Review
- Histone Methylation and Chromatin Remodeling in Non-Small Cell Lung Cancer: Mechanisms of Oncogenesis and Emerging Therapeutic Strategies.Biomedicines · 2026Review
- Epigenetic modifications in cancer drug resistance: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Epigenetic Gatekeeping of Intestinal Stem Cell Transformation.bioRxiv : the preprint server for biology · 2026Article
- Developmental stage and cellular context determine oncogenic and molecular outcomes ofBlood neoplasia · 2025Article
- Treating human cancer by targeting EZH2.Genes & diseases · 2025Review
- Immunoexpressions of PD-L1 and EZH2 in Endometrial Carcinoma: Associations with Clinicopathological Parameters.Diagnostics (Basel, Switzerland) · 2025Article
- Targeting the epigenome and tumor heterogeneity: advances in immunotherapy for chemoresistant metastatic colorectal cancer.Frontiers in immunology · 2025Review
- Exploring oncogenic roles and clinical significance of EZH2: focus on non-canonical activities.Therapeutic advances in medical oncology · 2025Review
- Stat3-mediated Atg7 expression regulates anti-tumor immunity in mouse melanoma.Cancer immunology, immunotherapy : CII · 2024Article
- Dual-target EZH2 inhibitor: latest advances in medicinal chemistry.Future medicinal chemistry · 2024Review
- Stat3-mediated Atg7 expression enhances anti-tumor immunity in melanoma.bioRxiv : the preprint server for biology · 2024Article
- The therapeutic potential of targeting the CHD protein family in cancer.Pharmacology & therapeutics · 2024Review
- First-in-Class Dual EZH2-HSP90 Inhibitor Eliciting Striking Antiglioblastoma ActivityJournal of medicinal chemistry · 2024Article
- Glucose Deprivation Promotes Pseudohypoxia and Dedifferentiation in Lung Adenocarcinoma.Cancer research · 2024Article
- Insight into the Inhibitory Mechanism of Embryonic Ectoderm Development Subunit by Triazolopyrimidine Derivatives as Inhibitors through Molecular Dynamics Simulation.Molecules (Basel, Switzerland) · 2023Article
- Phosphorylation of EZH2 differs HER2-positive breast cancer invasiveness in a site-specific manner.BMC cancer · 2023Article
- CUL4B functions as a tumor suppressor in KRAS-driven lung tumors by inhibiting the recruitment of myeloid-derived suppressor cells.Oncogene · 2023Article
- Identification of a polycomb group-related gene signature for predicting prognosis and immunotherapy efficacy in lung adenocarcinoma.Journal of thoracic disease · 2023Article
11 more citing papers are in PubMed but not listed here.
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Authors and funding
31 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledAs a master regulator of chromatin function, the lysine methyltransferase EZH2 orchestrates transcriptional silencing of developmental gene networks. Overexpression of EZH2 is commonly observed in human epithelial cancers, such as non-small cell lung carcinoma (NSCLC), yet definitive demonstration of malignant transformation by deregulated EZH2 remains elusive. Here, we demonstrate the causal role of EZH2 overexpression in NSCLC with new genetically engineered mouse models of lung adenocarcinoma. Deregulated EZH2 silences normal developmental pathways, leading to epigenetic transformation independent of canonical growth factor pathway activation. As such, tumors feature a transcriptional program distinct from KRAS- and EGFR-mutant mouse lung cancers, but shared with human lung adenocarcinomas exhibiting high EZH2 expression. To target EZH2-dependent cancers, we developed a potent open-source EZH2 inhibitor, JQEZ5, that promoted the regression of EZH2-driven tumors in vivo, confirming oncogenic addiction to EZH2 in established tumors and providing the rationale for epigenetic therapy in a subset of lung cancer. SIGNIFICANCE: EZH2 overexpression induces murine lung cancers that are similar to human NSCLC with high EZH2 expression and low levels of phosphorylated AKT and ERK, implicating biomarkers for EZH2 inhibitor sensitivity. Our EZH2 inhibitor, JQEZ5, promotes regression of these tumors, revealing a potential role for anti-EZH2 therapy in lung cancer. Cancer Discov; 6(9); 1006-21. ©2016 AACR.See related commentary by Frankel et al., p. 949This article is highlighted in the In This Issue feature, p. 932.
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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.