ChIP-seq data for H3K27me3 from human lymphoma cell lines
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA470709 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7140800_1.fastq.gz | Fastqsanger.gz | |||
| SRR7140800_2.fastq.gz | Fastqsanger.gz | |||
| SRR7140793_1.fastq.gz | Fastqsanger.gz | |||
| SRR7140793_2.fastq.gz | Fastqsanger.gz | |||
| SRR7140794_1.fastq.gz | Fastqsanger.gz |
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Project description:ChIP-seq experiments for H3K27me3 histone mark were performed on OCI-Ly19 EZH2-wild type cell line (LY19WT) and a syngenic OCI-Ly19 cell line expressing the mutated protein EZH2-Y646F (LY19Y646F). We investigated the genome-wide changes in H3K27me3 levels between the two conditions.
2019-01-01 | GSE114264 | GEO
Project description:IRF8, a transcriptional factor, has the heightened expression in germinal center(GC) B cell and GC-origin B cell lymphoma. To identify IRF8 direct targets in GC B cells, ChIP-chip ananlysis was done in three different GC-origin diffuse large B cell lymphoma cell lines. IRF8-negative cell lines, MMS1, was also used as a negatvie control.
2011-10-15 | GSE30357 | GEO
Project description:ChIP-seq and RNA-seq from human lymphoma cell lines
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Project description:IRF8, a transcriptional factor, has the heightened expression in germinal center(GC) B cell and GC-origin B cell lymphoma. To identify IRF8 direct targets in GC B cells, ChIP-chip ananlysis was done in three different GC-origin diffuse large B cell lymphoma cell lines. IRF8-negative cell lines, MMS1, was also used as a negatvie control. IRF8 ChIP in three different cell lines (ODH1, VAL and LY1:high level of IRF8) and in one negative control cell lines (MMS1:negatvie for IRF8). Total four different samples. One sample per a set of two arrays (promoter1 and promoter2).
2011-10-14 | E-GEOD-30357 | biostudies-arrayexpress
Project description:RNA-seq data from human lymphoma cell lines
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Project description:In eukaryotes, epigenetic post-translational modification of histones is critical for regulation of chromatin structure and gene expression. EZH2 is the catalytic subunit of the Polycomb Repressive Complex 2 (PRC2) and is responsible for repressing target gene expression through methylation of histone H3 on lysine 27 (H3K27). Over-expression of EZH2 is implicated in tumorigenesis and correlates with poor prognosis in multiple tumor types. Recent reports have identified somatic heterozygous mutations of Y641 and A677 residues within the catalytic SET domain of EZH2 in diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL). The Y641 residue is the most frequently mutated residue, with 22% of GCB (Germinal centre B-cell) DLBCL and FL harboring mutations at this site. These lymphomas exhibit increased H3K27 tri-methylation (H3K27me3) due to altered substrate preferences of the mutant enzymes. However, it is unknown whether direct inhibition of EZH2 methyltransferase activity alone will be effective in treating lymphomas carrying activating EZH2 mutations. Herein, we demonstrate that GSK126, a potent, highly-selective, SAM-competitive, small molecule inhibitor of EZH2 methyltransferase activity, decreases global H3K27me3 levels and reactivates silenced PRC2 target genes. GSK126 effectively inhibits the proliferation of EZH2 mutant DLBCL cell lines and dramatically inhibits the growth of EZH2 mutant DLBCL xenografts in mice. Together, these data demonstrate that pharmacological inhibition of EZH2 activity may provide a promising treatment for EZH2 mutant lymphoma. We performed a ChIP-seq experiment to understand the genomewide pattern of H3K27me3 enrichment in DLBCL cell lines that were differentially sensitive to GSK126. H3K27me3 bound chromatin and input controls was immunoprecipitated and subjected to sequencing on the Illumina GA Iix. In total, 3 cell lines were profiled - 3 EZH2 mutant (Pfeiffer, KARPAS-422, WSU-DLCL2).
2012-10-12 | E-GEOD-40970 | biostudies-arrayexpress
Project description:IRF8, a transcriptional factor, has the heightened expression in germinal center(GC) B cell and GC-origin B cell lymphoma. To identify IRF8 direct targets in GC B cells, ChIP-chip ananlysis was done in three different GC-origin diffuse large B cell lymphoma cell lines. IRF8-negative cell lines, MPC11, was also used as a negatvie control.
2011-10-15 | GSE30519 | GEO
Project description:H3K27me3 in vitro ChIP-Sequencing data [H3K27me3_PA_SCC25]
| PRJNA627210 | ENA
Project description:IRF8, a transcriptional factor, has the heightened expression in germinal center(GC) B cell and GC-origin B cell lymphoma. To identify IRF8 direct targets in GC B cells, ChIP-chip ananlysis was done in three different GC-origin diffuse large B cell lymphoma cell lines. IRF8-negative cell lines, MPC11, was also used as a negatvie control. IRF8 ChIP in three different cell lines (NFS201, NFS202 and NFS205:high level of IRF8) and in one negative control cell lines(MPC11:negatvie for IRF8). Total four different samples. One sample per a set of two arrays (promoter1 and promoter2).
2011-10-14 | E-GEOD-30519 | biostudies-arrayexpress
Project description:Mutations within the catalytic domain of the histone methyltransferase (HMT) EZH2 have been identified in subsets of Non-Hodgkin Lymphoma (NHL) patients. These genetic alterations are hypothesized to confer an oncogenic dependency on EZH2 enzymatic activity in these cancers. We previously reported the discovery of a potent, selective, S-adenosyl-methionine-competitive and orally bioavailable small molecule inhibitor of EZH2, EPZ-6438. EPZ-6438 selectively inhibits intracellular lysine 27 of histone H3 (H3K27) methylation in a concentration- and time-dependent manner in both EZH2 wild type and mutant lymphoma cells. Inhibition of H3K27 trimethylation (H3K27Me3) led to selective cell killing of human lymphoma cell lines bearing EZH2 catalytic domain point mutations. Treatment of xenograft-bearing mice with EPZ-6438 leads to dose-dependent tumor growth inhibition and eradication of genetically altered NHL with correlative diminution of H3K27Me3 levels in tumors and selected normal tissues. Mice dosed orally with EPZ-6438 for 28 days remained tumor free for up to 63 day after stopping compound treatment in two EZH2 mutant xenograft models. These data confirm the dependency of mutant NHL on EZH2 activity and portend the utility of EZH2-targeted drugs for the treatment of these genetically defined cancers. To identify potential biomarker and gain mechanistic insights in EPZ6438 treated lymphoma, lymphoma cell lines with or without EZH2 Y641 mutation were treated with EPZ6438 at Lowest Cytotoxic Concentration (LCC) and 10xLCC. Transcriptomes were profiled on Affemetrix U133 Plus2 chips. Differentially expressed genes and pathways upon compound treatment were anayzed. Lymphoma cell lines WSU-DLCL2, SU-DHL6, Pfeiffer, and Karpas422 were treated by EPZ6438 for 2 days, 4 days and 6 days. Treatment doses are LCC and 10xLCC of each cell lines. KARPAS_422, SUDHL6, and WSU_DLCL2 have the EZH2 Y641 mutation. PFEIFFER does not have the EZH2 Y641 mutation.
2014-02-19 | E-GEOD-49284 | biostudies-arrayexpress