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Inhibition of a G9a/DNMT network triggers an immune-mediated bladder cancer regression treated with CM272 (IC50)

ABSTRACT: Based on the identification of G9a as a potential target in BC, we decided to test the effect of a recently described dual inhibitor against G9a/DNMTs, CM-272, in several BC cell lines

ORGANISM(S): Homo sapiens

PROVIDER: GSE115544 | GEO | 2019/02/01

REPOSITORIES: GEO

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Inhibition of a G9a/DNMT network triggers an immune-mediated bladder cancer regression

Project description:Using a novel immunocompetent quadruple (PtenF/F; Trp53F/F; Rb1F/F;Rbl1-/-) knockout transgenic mouse model of highly aggressive metastatic muscle-invasive BC, we demonstrate that treatment with CM272 and CDDP results in a significant tumor and metastasis regression with a very significant prolonged survival

2019-02-01 | GSE115485 | GEO

Discovery of first-in-class reversible dual small molecule inhibitors against G9a and DNMTs with in vivo activity in hematological malignancies [array]

Project description:The indisputable role of epigenetics in cancer and the fact that epigenetic alterations can be reversed have favored development of epigenetic drugs. In this study, we have design and synthesize potent novel, selective and reversible chemical probes that simultaneously inhibit the G9a and DNMTs methyltransferase activity. In vitro treatment of hematological neoplasia (Acute Myeloid Leukemia-AML, Acute Lymphoblastic Leukemia-ALL and Diffuse Large B-cell Lymphoma-DLBCL) with the lead compound CM-272, inhibited cell proliferation and promoted apoptosis, inducing interferon stimulated genes and immunogenic cell death. CM-272 significantly prolonged survival of AML, ALL and DLBCL xenogeneic models. Our results represent the discovery of first-in-class dual inhibitors of G9a/DNMTs and establish this chemical series, as a promising therapeutic tool for unmet needs in hematological tumors.

2017-08-11 | GSE78517 | GEO

Discovery of first-in-class reversible dual small molecule inhibitors against G9a and DNMTs with in vivo activity in hematological malignancies [RNA-Seq]

Project description:The indisputable role of epigenetics in cancer and the fact that epigenetic alterations can be reversed have favored development of epigenetic drugs. In this study, we have designed and synthesized potent novel, selective and reversible chemical probes that simultaneously inhibit the G9a and DNMTs methyltransferase activity. In vitro treatment of hematological neoplasia (Acute Myeloid Leukemia-AML, Acute Lymphoblastic Leukemia-ALL and Diffuse Large B-cell Lymphoma-DLBCL) with the lead compound CM-272, inhibited cell proliferation and promoted apoptosis, inducing interferon stimulated genes and immunogenic cell death. CM-272 significantly prolonged survival of AML, ALL and DLBCL xenogeneic models. Our results represent the discovery of first-in-class dual inhibitors of G9a/DNMTs and establish this chemical series, as a promising therapeutic tool for unmet needs in hematological tumors.

2017-08-11 | GSE78930 | GEO

Inhibition of a G9a/DNMT network triggers an immune-mediated bladder cancer regression

Project description:Inhibition of a G9a/DNMT network triggers an immune-mediated bladder cancer regression

| PRJNA475147 | ENA

Inhibition of a G9a/DNMT network triggers an immune-mediated bladder cancer regression treated with CM272 (IC50)

Project description:Inhibition of a G9a/DNMT network triggers an immune-mediated bladder cancer regression treated with CM272 (IC50)

| PRJNA475304 | ENA

Expression data from bladder cancer cells T24 - treated with G9a siRNA or negative control siRNA

Project description:Target genes regulated by G9a in bladder cancer cells T24 In this dataset, we include the expression data obtained from bladder cancer cells T24 treated with G9a siRNA or negative control siRNA. These data are used to obtain genes that are differentially expressed in response to G9a konckdown.

2019-05-29 | GSE115341 | GEO

Identification of proteins stably associated with G9a/GLP (EHMT2/EHMT1) complex of histone methyltransferases

Project description:G9a (EHMT2) and the G9a-like protein GLP (EHMT1) form a stable G9a/GLP heterodimer in embryonic stem cells and function cooperatively to establish and maintain the abundant repressive H3K9me2 modification, in addition to modifying several non-histone proteins. The G9a-dependent H3K9me2 is implicated in lineage-specific gene silencing and covers large chromosomal domains. While the mechanism of H3K9me2maintenance by G9a/GLP is known, how new patterns of this modification are established is not well understood. With this in mind, we used FLAG affinity purification of G9a under two different stringency conditions (150 and 300 mM NaCl) coupled with mass spectrometry to identify proteins stably associated with G9a/GLP, which could serve as potential recruiters of the complex to unmodified chromatin.

2016-03-16 | PXD003466 | Pride

Transcription profiling of mouse embryonic fibroblasts deleted for G9a reconstituted with empty vector (delta), wild type FLAG-G9a (WT), FLAG-G9a K165A (K165A) or FLAG-G9a H1093K catalytic mutant reveasl methylation of hMTase G9a on a histone-like site regulates protein complex assembly

Project description:Gene expression in eukaryotes is tightly linked to the methylation state of specific lysine residues within the N-terminal region of the core histone proteins. While the mechanisms connecting histone lysine methylation to effector protein recruitment and control of gene activity are increasingly well understood, it remains unknown whether non-histone chromatin proteins are targets for similar modification-recognition systems. Here we show that histone H3 and the H3 methyltransferase G9a share a conserved methylation motif that is both necessary and sufficient to mediate in vivo interaction with the potent epigenetic regulator Heterochromatin Protein 1 (HP1). As with H3, G9a-HP1 interaction is dependent on lysine methylation and can be reversed by adjacent phosphorylation. NMR analysis demonstrates that the HP1 chromodomain recognizes methyl-G9a through a binding mode similar to that used in recognition of methyl-H3, and that adjacent phosphorylation directly antagonizes G9a-HP1 interaction. In addition to uncovering the chromodomain as a generalized methyl-lysine binding module, these data identify histone-like modification cassettes (or âhistone mimicsâ) as an entirely new class of non-histone methylation targets, and directly demonstrate the relevance of the principles underlying the histone code to the regulation of non-histone proteins. Experiment Overall Design: Two independent Affymetrix gene expression microarray analyses were performed on samples from G9a-deleted MEFs reconstituted with empty vector (delta), wild type FLAG-G9a (WT), FLAG-G9a K165A (K165A) or FLAG-G9a H1093K catalytic mutant (H1093K).

2008-06-15 | E-GEOD-8011 | biostudies-arrayexpress

H3K9me3 abcam.D.mel 3rd Instar Larvae Nuclei G9a mutant.Affy 2

Project description:modENCODE_submission_5611 This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: G9a mutant (official name : G9a mutant genotype : G9a[RG5]/G9a[RG5] outcross : 3 transgene : n/a tags : homologous recombination tag : none description : Mutation generated by end-out homologous recombination at the G9a locus. The entire open reading frame of G9a has been removed. Developmental Stage: 3rd Instar Larvae; Genotype: G9a[RG5]/G9a[RG5]; Transgene: n/a; NUMBER OF REPLICATES: 4; EXPERIMENTAL FACTORS: Strain G9a mutant (official name : G9a mutant genotype : G9a[RG5]/G9a[RG5] outcross : 3 transgene : n/a tags : homologous recombination tag : none description : Mutation generated by end-out homologous recombination at the G9a locus. The entire open reading frame of G9a has been removed. Antibody H3K9me3 abcam (target is H3K9me3); Developmental Stage 3rd Instar Larvae

2013-03-13 | E-GEOD-45102 | biostudies-arrayexpress

H3K36me3 abcam.D.mel 3rd Instar Larvae Nuclei G9a mutant.Affy 2

Project description:modENCODE_submission_5615 This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: G9a mutant (official name : G9a mutant genotype : G9a[RG5]/G9a[RG5] outcross : 3 transgene : n/a tags : homologous recombination tag : none description : Mutation generated by end-out homologous recombination at the G9a locus. The entire open reading frame of G9a has been removed. Developmental Stage: 3rd Instar Larvae; Genotype: G9a[RG5]/G9a[RG5]; Transgene: n/a; NUMBER OF REPLICATES: 4; EXPERIMENTAL FACTORS: Strain G9a mutant (official name : G9a mutant genotype : G9a[RG5]/G9a[RG5] outcross : 3 transgene : n/a tags : homologous recombination tag : none description : Mutation generated by end-out homologous recombination at the G9a locus. The entire open reading frame of G9a has been removed. Antibody H3K36me3 abcam (target is H3K36me3); Developmental Stage 3rd Instar Larvae

2013-03-06 | E-GEOD-44894 | biostudies-arrayexpress

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