Gene silencing in cancer by histone H3 lysine 27 trimethylation independent of promoter DNA methylation

By Y. Kondo, Lanlan Shen, A. S. Cheng, Saira S. Ahmed, Y. Boumber, Chantale Charo, T. Yamochi, T. Urano, K. Furukawa, B. Kwabi-Addo and 4 more. Nature Genetics, 2008

641 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/1f2fb589e8299eb5c416fb68cad1a8995fa70b23

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In Molecular Biology

1. Peter A. Jones
2. S. Baylin
3. Manel Esteller
4. T. Kelly
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7. Daniel D. De Carvalho
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Citations in the corpus

• DNA methylation and cancer. (2010, background): “Moreover, it was also reported that in cancer cells up to 5% of promoters containing CpGs were silenced by H3K27 trimethylation which was independent of DNA methylation (Kondo et al., 2008).”
• Somatic mutations at EZH2 Y641 act dominantly through a mechanism of selectively altered PRC2 catalytic activity, to increase H3K27 trimethylation. (2011, background): “2 M biotinylated peptide substrate (ie, peptide mimicking the H3 tail, H3(21-44)), which has been unmethylated (H3K27me0, open bar or me0), monomethylated (H3K27me1, gray bar or me1) or dimethylated (H3K27me2, black bar or me2) at Lys-27.”
• Gene Body Methylation can alter Gene Expression and is a Therapeutic Target in Cancer (2014, background): “Both of thesemarks are considered antagonistic to DNA methylation, which might explain why they were refractory to rebound methylation (Gal-Yam et al., 2008; Kondo et al., 2008; Zilberman et al., 2008).”
• Repression of E-cadherin by the polycomb group protein EZH2 in cancer (2008, background): “A recent study by Kondo et al. (2008) suggests that gene silencing by histone H3 lysine K27 trimethylation is independent of promoter DNA methylation.”
• DZNep Is a Global Histone Methylation Inhibitor that Reactivates Developmental Genes Not Silenced by DNA Methylation (2009, background): “The first is the well-known silencing of genes by DNA methylation (5) and the second is the silencing of genes mediated by the Polycomb repressor complex 2, which is often independent of DNA methylation (6, 7).”
• Inactivating mutations of the histone methyltransferase gene EZH2 in myeloid disorders (2010, background): “Trimethylated H3 (H3K27me3) serves as a signal for recruitment of further proteins, including the polycomb repressive complex 1 (PRC1), which maintains a silenced state by mechanisms that may or may not require DNA methylatio”
• Molecular genetics of prostate cancer: new prospects for old challenges. (2010, background): “Furthermore, prostate tumors display global changes in chromatin modification coincident with cancer progression (Kondo et al. 2008; Ke et al. 2009) that presumably result in significant perturbations in the gene expression program of tumor cells.”
• Reduced H3K27me3 and DNA hypomethylation are major drivers of gene expression in K27M mutant pediatric high-grade gliomas. (2013, result): “This is consistent with other studies reporting on PRC2-mediated gene silencing independent of DNA hypermethylation (Kondo et al., 2008).”
• Rethinking how DNA Methylation Patterns are Maintained (2009, background): “, but the recruitment of DNMT1 and DNMT3A by EZH2 is not as well substantiate”
• A decade of exploring the cancer epigenome — biological and translational implications (2011, background): “Intriguingly, as discussed below, these gene promoters are prone to undergoing an epigenetic switc”