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Keywords {🔍}

ezh, cancer, pubmed, article, google, scholar, cells, cas, cell, tumor, expression, central, histone, gene, activity, protein, prc, complex, hkme, breast, progression, functions, transcriptional, regulation, methyltransferase, proliferation, function, promotes, inhibitors, methylation, inhibition, identified, mutations, lymphoma, growth, directly, epigenetic, roles, genes, nat, studies, development, targeting, prostate, demonstrated, invasion, polycomb, glioblastoma, silencing, phosphorylation,

Topics {✒️}

ifn-γ-producing pd-1low cd8+ natural killer/t-cell lymphoma parp-mediated poly-adp ribosylation article download pdf nk-based cancer immunotherapies polycomb-dependent epigenetic landscape e3 ubiquitin ligase dna-damage repair deficiency adult t-cell leukemia hypoxia-induced hif-1α pd-l1 checkpoint blockade cdk5/fbw7-dependent ubiquitination disabled homolog2-interacting protein adoptive t-cell transfusion castration-resistant prostate cancer indicating mir-26a-ezh2 axis dual-faced molecule acting hifi-alpha activation underlies histone-modified hypomethylated gene ezh2-mediated epigenetic silencing enhances cisplatin-induced apoptosis cells-mediated tumor surveillance ubiquitination-dependent protein degradation mirna-mediated post-transcriptional regulation ezh2/forkhead box m1 triple-negative breast cancer activation ofhif-1α results type chemokines cxcl9 ezh2-mediated gene silencing cdk-mediated ezh2 phosphorylation increasing ezh2-mediated overexpression chromatin-modifying enzyme ezh2 exhibiting anti-tumor effects natural killer cells prc2-independent gene transactivation ezh2-mediated drug resistance ezh2-deficient tregs fail b-cell lymphomas histone h3k27 trimethylation mir-26a-ezh2 axis mds-mpn overlap disorders increase ezh2-mediated h3k27me3 jak2-mediated phosphorylation inhibit anti-tumor immunity mir-26a inhibits ezh2 full access ring1b ubiquitin ligases renal cell carcinoma weijian guo androgen receptor-target genes

Questions {❓}

• EZH2 in cancer progression and potential application in cancer therapy: a friend or foe?

Schema {🗺️}

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         headline:Epigenetic regulation of cancer progression by EZH2: from biological insights to therapeutic potential
         description:Enhancer of zeste homolog 2 (EZH2), a histone methyltransferase and a catalytic component of PRC2, catalyzes tri-methylation of histone H3 at Lys 27 (H3K27me3) to regulate gene expression through epigenetic machinery. EZH2 also functions both as a transcriptional suppressor and a transcriptional co-activator, depending on H3K27me3 or not and on the different cellular contexts. Unsurprisingly, numerous studies have highlighted the role of EZH2 in cancer development and progression. Through modulating critical gene expression, EZH2 promotes cell survival, proliferation, epithelial to mesenchymal, invasion, and drug resistance of cancer cells. The tumor suppressive effects of EZH2 are also identified. What is more, EZH2 has decisive roles in immune cells (for example, T cells, NK cells, dendritic cells and macrophages), which are essential components in tumor microenvironment. In this review, we aim to discuss the molecular functions of EZH2, highlight recent findings regarding the physiological functions and related regulation of EZH2 in cancer pathogenesis. Furthermore, we summarized and updated the emerging roles of EZH2 in tumor immunity, and current pre-clinical and clinical trials of EZH2 inhibitors in cancer therapy.
         datePublished:2018-03-09T00:00:00Z
         dateModified:2018-03-09T00:00:00Z
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            Epigenetic
            Histone H3 Lys27 trimethylation
            Cancer
            Polycomb repressive complex
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            general
            Cancer Research
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      headline:Epigenetic regulation of cancer progression by EZH2: from biological insights to therapeutic potential
      description:Enhancer of zeste homolog 2 (EZH2), a histone methyltransferase and a catalytic component of PRC2, catalyzes tri-methylation of histone H3 at Lys 27 (H3K27me3) to regulate gene expression through epigenetic machinery. EZH2 also functions both as a transcriptional suppressor and a transcriptional co-activator, depending on H3K27me3 or not and on the different cellular contexts. Unsurprisingly, numerous studies have highlighted the role of EZH2 in cancer development and progression. Through modulating critical gene expression, EZH2 promotes cell survival, proliferation, epithelial to mesenchymal, invasion, and drug resistance of cancer cells. The tumor suppressive effects of EZH2 are also identified. What is more, EZH2 has decisive roles in immune cells (for example, T cells, NK cells, dendritic cells and macrophages), which are essential components in tumor microenvironment. In this review, we aim to discuss the molecular functions of EZH2, highlight recent findings regarding the physiological functions and related regulation of EZH2 in cancer pathogenesis. Furthermore, we summarized and updated the emerging roles of EZH2 in tumor immunity, and current pre-clinical and clinical trials of EZH2 inhibitors in cancer therapy.
      datePublished:2018-03-09T00:00:00Z
      dateModified:2018-03-09T00:00:00Z
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      sameAs:https://doi.org/10.1186/s40364-018-0122-2
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         EZH2
         Epigenetic
         Histone H3 Lys27 trimethylation
         Cancer
         Polycomb repressive complex
         Biomedicine
         general
         Cancer Research
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            name:Fudan University
            address:
               name:Department of Oncology, Shanghai Medical college, Fudan University, Shanghai, China
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      name:Qian Li
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            name:Fudan University
            address:
               name:Department of Oncology, Shanghai Medical college, Fudan University, Shanghai, China
               type:PostalAddress
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            name:Fudan University
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      name:Yi Feng
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               name:Department of Oncology, Shanghai Medical college, Fudan University, Shanghai, China
               type:PostalAddress
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      name:Tianshu Liu
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               type:PostalAddress
            type:Organization
            name:Fudan University
            address:
               name:Department of Medical Oncology, Zhongshan Hospital, Fudan University, Shanghai, China
               type:PostalAddress
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      name:Weijian Guo
      url:http://orcid.org/0000-0003-3078-3539
      affiliation:
            name:Fudan University Shanghai Cancer Center
            address:
               name:Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, China
               type:PostalAddress
            type:Organization
            name:Fudan University
            address:
               name:Department of Oncology, Shanghai Medical college, Fudan University, Shanghai, China
               type:PostalAddress
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      email:[email protected]
PostalAddress:
      name:Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, China
      name:Department of Oncology, Shanghai Medical college, Fudan University, Shanghai, China
      name:Department of Medical Oncology, Zhongshan Hospital, Fudan University, Shanghai, China
      name:Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, China
      name:Department of Oncology, Shanghai Medical college, Fudan University, Shanghai, China
      name:Department of Oncology, Shanghai Medical college, Fudan University, Shanghai, China
      name:Department of Medical Oncology, Zhongshan Hospital, Fudan University, Shanghai, China
      name:Department of Oncology, Shanghai Medical college, Fudan University, Shanghai, China
      name:Department of Medical Oncology, Zhongshan Hospital, Fudan University, Shanghai, China
      name:Department of Oncology, Shanghai Medical college, Fudan University, Shanghai, China
      name:Department of Medical Oncology, Zhongshan Hospital, Fudan University, Shanghai, China
      name:Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, China
      name:Department of Oncology, Shanghai Medical college, Fudan University, Shanghai, China

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