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H3K9 Trimethylation Silences Fas Expression to Confer Colon Carcinoma Immune Escape and 5-Fluorouracil Chemoresistance

ABSTRACT: We have determined that verticillin A is a histone methyltransfease inhibitor that selectively inhibits human SUV39H1, SUV39H2, G9a and GLP to inhibit H3K9 methylation in human colon cancer cells. The objective here is to identify verticillin A target genes in human colon cancer cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE51262 | GEO | 2015/04/01

SECONDARY ACCESSION(S): PRJNA222251

REPOSITORIES: GEO

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H3K9 Trimethylation Silences Fas Expression To Confer Colon Carcinoma Immune Escape and 5-Fluorouracil Chemoresistance.

Project description: Not available

| S-EPMC4530033 | biostudies-literature

Verticillin A is a selective HMTase inhibitor that inhibit H3K9 methylation to overcome chemoresistance of human colon carcinoma

Project description:We have determined that verticillin A is a histone methyltransfease inhibitor that selectively inhibits human SUV39H1, SUV39H2, G9a and GLP to inhibit H3K9 methylation in human colon cancer cells. The objective here is to identify verticillin A target genes in human colon cancer cells. 5-FU-resistant human colon carcinoma cell lines LS411N-5FU-R was established from the metastatic human colon carcinoma cell line LS411N. LS411N-5FU-R cells were cultured in the absence or presence of verticillin A (50 nM) for 3 days and used for RNA lsolation. DNA microarray analysis was done in replicates in the Georgia Regents University Cancer Center Genomic Core Facility.

2015-04-01 | E-GEOD-51262 | biostudies-arrayexpress

Specificity, propagation and memory of pericentric heterochromatin in mouse fibroblasts

Project description:We assembled a quantitative map for the abundance and interactions of 16 factors related to PCH in living cells and found that stably bound complexes of the histone methyltransferase Suv39h1/2 demarcate the PCH state. From the experimental data we developed a predictive mathematical model that explains how chromatin-bound Suv39h1/2 complexes act as nucleation sites and propagate a spatially confined PCH domain with elevated histone H3 trimethylation levels via chromatin dynamics. Enrichment of HP1, Suv39h1/h2, H3K9me3 and H3K36me3 was assessed by ChIP-seq in NPCs derived from ESCs showing differential occupation at intergenic major satellite repeats and enrichment of heterochromatin factors. ChIP-seq of HP1, Suv39h1, Suv39h2, H3K9me3, H3K36me3 in NPCs

2014-08-12 | E-GEOD-58555 | biostudies-arrayexpress

Loss of H3K9 tri-methylation alters chromosome compaction and transcription factor retention during mitosis

Project description:Recent studies have shown that repressive chromatin machinery, including DNA methyltransferases and Polycomb Repressor Complexes, bind to chromosomes throughout mitosis and their depletion results in increased chromosome size. Here we show that enzymes that catalyse H3K9 methylation, such as Suv39h1, Suv39h2, G9a and Glp, are also retained on mitotic chromosomes. Surprisingly however, mutants lacking H3K9me3 have unusually small and compact mitotic chromosomes associated with increased H3S10ph and H3K27me3 levels. Chromosome size and centromere compaction in these mutants were rescued by providing exogenous Suv39h1, or inhibiting Ezh2 activity. Quantitative proteomic comparisons of native mitotic chromosomes isolated from wildtype versus Suv39h1/Suv39h2 double-null mouse ESCs revealed that H3K9me3 was essential for the efficient retention of bookmarking factors such as Esrrb. These results highlight an unexpected role for repressive heterochromatin domains in preserving transcription factor binding through mitosis, and underscore the importance of H3K9me3 for sustaining chromosome architecture and epigenetic memory during cell division.

2023-01-25 | PXD039521 | Pride

RNA-seq profiles of DP thymocytes from control and Suv39h1/Suv39h2 double knockout mice

Project description:H3K9me3-dependent heterochromatin is critical for the silencing of repeat-rich pericentromeric regions and also has key roles in repressing lineage-inappropriate protein-coding genes for healthy cellular function. Here we investigate the transcriptomic effects of heterochromatin loss in primary immune cells deficient in both Suv39h1 and Suv39h2 (Suv39DKO), the major mammalian histone methyltransferase enzymes which catalyse heterochromatic H3K9me3 deposition.

2024-03-27 | GSE156296 | GEO

Loss of H3K9 tri-methylation alters mitotic chromosome compaction and transcription factor retention during mitosis

Project description:Recent studies have shown that repressive chromatin machinery, including DNA methyltransferases (DNMTs) and Polycomb Repressor Complexes (PRCs), bind to chromosomes throughout mitosis and their depletion results in increased chromosome size. Enzymes that catalyse H3K9 methylation, such as Suv39h1, Suv39h2, G9a, GLP are also retained by mitotic chromosomes. Surprisingly however, mutants lacking H3K9me3 have unusually small and compact mitotic chromosomes that are associated with increased H3S10ph and H3K27me3 levels. Chromosome size and centromere compaction in these mutants was rescued by providing exogenous Suv39h1, or inhibiting Ezh2 activity. Quantitative proteomic comparisons of native mitotic chromosomes isolated from wildtype versus Suv39h1,2 double null ESCs revealed that H3K9me3 was essential for the efficient retention of bookmarking factors such as Esrrb. These results highlight an unexpected role for repressive heterochromatin domains in preserving transcription factor binding through mitosis, and underscore the importance of H3K9me3 for sustaining chromosome architecture and epigenetic memory during cell division.

2022-10-12 | PXD030771 | Pride

in situ Hi-C profiles of DP thymocyltes from control and Suv39h1/Suv39h2 double knockout mice

Project description:H3K9me3-dependent heterochromatin is critical for the silencing of repeat-rich pericentromeric regions and also has key roles in repressing lineage-inappropriate protein-coding genes for healthy cellular function. Here we investigate the disruption of genome organization in the absence of H3K9me3-dependent heterochromatin by performing in situ Hi-C in primary immune cells deficient in both Suv39h1 and Suv39h2 (Suv39DKO), the major mammalian histone methyltransferase enzymes which catalyse heterochromatic H3K9me3 deposition.

2024-03-27 | GSE156294 | GEO

Elevated XIAP expression alone does not confer chemoresistance.

Project description: Not available

| S-EPMC2883704 | biostudies-literature

RNA-seq, LaminB1 ChIP-seq and in situ Hi-C of double positive thymocytes from control and Suv39h1/Suv39h2 double knockout mice

Project description:H3K9me3-dependent heterochromatin is critical for the silencing of repeat-rich pericentromeric regions and also has key roles in repressing lineage-inappropriate protein-coding genes for healthy cellular function. Within all eukaryotic nuclei, heterochromatin and euchromatin are spatially segregated, with euchromatin typically located in the nuclear interior and heterochromatin at the nuclear periphery. We investigated the effects of loss of H3K9me3-dependent heterochromatin in primary immune cells deficient in both Suv39h1 and Suv39h2 (Suv39DKO), the major mammalian histone methyltransferase enzymes which catalyse heterochromatic H3K9me3 deposition.

2024-03-27 | GSE156297 | GEO

Transcriptomic analysis in Suv39h2-deficient brain during early neurodevelopment

Project description:To examine the molecular phenotype of Suv39h2-deficits during early neurodevelopment, transcriptome analysis in the E11.5 brain of Suv39h2-deficient mouse and wild-type littermates were performed. The Suv39h2 mutation was made using CRISPR/Cas9n-mediated genome editing

2023-12-30 | E-MTAB-10528 | biostudies-arrayexpress

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