| PRC2 is a tumor suppressor in Emicro-myc lymphomagenesis, because disease onset was accelerated by heterozygosity for Suz12 or by short hairpin RNA-mediated knockdown of Suz12 or Ezh2. | lymphoma, |
| We show that, in contrast to PRC1, PRC2 is a tumor suppressor in Emicro-myc lymphomagenesis in lymphoma. | lymphoma, |
| Ezh2 Acts as a Tumor Suppressor in Kras-driven Lung Adenocarcinoma | lung, |
| The loss of Ezh2 in p53-null hematopoietic cells impeded the differentiation of early T cell precursors (ETPs) and eventually induced early T cell precursor acute lymphoblastic leukemia (ETP-ALL)-like disease, indicating that the polycomb repressive complex 2 functions as a tumor suppressor in ETPs. | leukemia, |
| overexpression of ZH2 could at least partially reverse the tumor suppressive effects of miR-31 indicating direct involvement of ZH2 in the miR-31 mediated inhibitory effects on advanced gastric cancer cell proliferation | gastric, |
| The knockdown of EZH2 phenocopied the tumor suppressive effects of miR-138 in cell models, whereas ectopic expression of EZH2 rescued the suppressive effects of miR-138. | None |
| EZH2 protein expression was associated with a tumor suppressor gene methylator phenotype. DNMT1, DNMT3B, and EZH2 were expressed at significantly higher levels in tumor vs. normal tissues. | None |
| Hyperactivation of EZH2 by mutations or amplification drives epigenetic silencing of genes involved in tumor suppression and immune responses in cancer | None |
| Mutating or deleting EZH2 can have both oncogenic and tumor suppressive functions by increasing or decreasing H3K27me3. (Review) | None |
| Data present convincing mechanistic results confirming the oncogenic function of EZH2 related to PRC2 functioning (repression of tumor suppressor genes through H3K27me3) in several biological models. | None |
| JAK2-V617F-expressing mice treated with an Ezh2 inhibitor showed higher platelet counts than vehicle controls. Our data support the proposed tumor suppressor function of EZH2 | None |
| the functional association between EZH2 expression and silencing of key tumor suppressor loci , was investigated. | None |
| EZH2 inhibits the expression of tumor suppressor gene RASSF2A via promoter hypermethylation. Thus, it plays an important role in tumorigenesis. | None |
| Inhibition of EZH2 down-regulates myeloma associated oncogenes and up-regulates microRNAs with potential tumor suppressor functions in multiple myeloma cells. | None |
| we report that AMPK phosphorylates the histone methyltransferase EZH2 at T311 to disrupt the interaction between EZH2 and SUZ12, another core component of the polycomb repressive complex 2 (PRC2), leading to attenuated PRC2-dependent methylation of histone H3 at Lys27. As such, PRC2 target genes, many of which are known tumor suppressors, were upregulated upon T311-EZH2 phosphorylation. | None |
| CARM1 promotes EZH2-mediated silencing of EZH2/BAF155 target tumor suppressor genes by methylating BAF155. | None |
| results show the effect of individual O-GlcNAcylation sites on the function of EZH2 and suggest an alternative approach to tumor suppression through selective inhibition of EZH2 O-GlcNAcylation. | None |
| Increased EZH2 expression correlates with oncogenesis of the bladder. | bladder, |
| Advanced cell- & animal imaging, expression profiling, stable siRNA-gene targeting, and TMAs of experimental and clinical samples indicate that activation of the Ezh2 oncogene-associated PcG pathway plays an essential role in metastatic prostate cancer. | prostate, |
| Essential role for activation of the Polycomb group (PcG) protein chromatin silencing pathway in metastatic prostate cancer. | prostate, |