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Chip-chip from Hepatocellular carcinoma (HCC) specimens with H3K4me3

ABSTRACT: Epigenetic changes commonly occur in hepatocellular carcinoma (HCC) and are associated with aberrant gene expression. Recently, we demonstrated the pivotal role of abnormal H3K4me3 methylation, which is catalyzed by the menin/MLL, a TrxG family, in HCC development. Meanwhile, there is clear evidence that increasing global levels of H3K27me3 are activated in human primary HCC. To further elucidate the functional relatedness of the active H3K4me3 and repressive H3K27me3 histone remodeling in HCC, we performed H3K4me3 and H3K27me3 ChIP-on-chip screen using three HCC specimens and their adjacent tissues.

ORGANISM(S): Homo sapiens

PROVIDER: GSE52190 | GEO | 2013/11/08

SECONDARY ACCESSION(S): PRJNA227135

REPOSITORIES: GEO

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Chip-chip from Hepatocellular carcinoma (HCC) specimens with H3K4me3

Project description:Epigenetic changes commonly occur in hepatocellular carcinoma (HCC) and are associated with aberrant gene expression. Recently, we demonstrated the pivotal role of abnormal H3K4me3 methylation, which is catalyzed by the menin/MLL, a TrxG family, in HCC development. Meanwhile, there is clear evidence that increasing global levels of H3K27me3 are activated in human primary HCC. To further elucidate the functional relatedness of the active H3K4me3 and repressive H3K27me3 histone remodeling in HCC, we performed H3K4me3 and H3K27me3 ChIP-on-chip screen using three HCC specimens and their adjacent tissues. Comparison of ChIP-on-chip results between tumor(C) and adjacent tissues(N) from three HCC specimens with H3K4me3

2013-11-08 | E-GEOD-52190 | biostudies-arrayexpress

Chip-chip from Hepatocellular carcinoma (HCC) specimens with H3K27me3

Project description:Epigenetic changes commonly occur in hepatocellular carcinoma (HCC) and are associated with aberrant gene expression. Recently, we demonstrated the pivotal role of abnormal H3K4me3 methylation, which is catalyzed by the menin/MLL, a TrxG family, in HCC development. Meanwhile, there is clear evidence that increasing global levels of H3K27me3 are activated in human primary HCC. To further elucidate the functional relatedness of the repressive H3K27me3 and active H3K4me3 histone remodeling in HCC, we performed H3K27me3 and H3K4me3 ChIP-on-chip screen using three HCC specimens and their adjacent tissues. Comparison of ChIP-on-chip results between tumor(C) and adjacent tissues(N) from three HCC specimens with H3K27me3

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Chip-chip from Hepatocellular carcinoma (HCC) specimens with H3K27me3

Project description:Epigenetic changes commonly occur in hepatocellular carcinoma (HCC) and are associated with aberrant gene expression. Recently, we demonstrated the pivotal role of abnormal H3K4me3 methylation, which is catalyzed by the menin/MLL, a TrxG family, in HCC development. Meanwhile, there is clear evidence that increasing global levels of H3K27me3 are activated in human primary HCC. To further elucidate the functional relatedness of the repressive H3K27me3 and active H3K4me3 histone remodeling in HCC, we performed H3K27me3 and H3K4me3 ChIP-on-chip screen using three HCC specimens and their adjacent tissues.

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Menin and H3K4me3 ChIP_Seq in mouse decidua

Project description:To detect the direct target genes of Menin and H3K4me3 in decidual stromal cells, decidual stromal cells are collected and subjected to ChIP-Seq. After aligned to mouse mm10 by STAR, peaks are called by MACS2. We found that Menin and H3K4me3 was significantly enriched at the transcription start site (TSS) of expressed genes (RPKM>1). A direct comparison of Menin and H3K4me3 ChIP-seq peaks at gene promoters showed a significantly strong positive correlation (R2=0.5888291). The promoters of 6,800 genes bound by Menin (92% of all genes with promoter bound by Menin) were also H3K4me3 modified.

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A cDNA microarray analysis was performed on HepG2 or L-02 cells with either vectors or constructs expressing MEN1

Project description:Menin, the product of the MEN1 gene in humans (Men1 in mice), is responsible for the inherited tumor syndrome, multiple endocrine neoplasia type 1 (MEN1). menin interacts with the trithorax group (trxG) proteins (Drosophila) and the mixed-lineage leukemia (MLL) (humans) histone methyltransferase (HMTase) complex, and it alters histone tail modifications and the transcription of target genes. To explore a potential functional implication of menin in HCC, we stably transfected HepG2 or L-02 cells with either vectors or constructs expressing MEN1. A cDNA microarray analysis was performed on HepG2 or L-02 cells with either vectors or constructs expressing MEN1. To obtain a broader understanding of the molecular network of menin in HCC, the whole genome microarray expression profiling was performed on HepG2 or L-02 cells with either vectors or constructs expressing MEN1. Comparison of gene expression results from HepG2 or L-02 cells with either vectors or constructs expressing MEN1.

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Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors (mRNA)

Project description:Inactivating mutations in the MEN1 gene predisposing to the multiple endocrine neoplasia type 1 (MEN1) syndrome can also cause sporadic pancreatic endocrine tumors. MEN1 encodes menin, a subunit of MLL1/MLL2-containing histone methyltransferase complexes that trimethylate histone H3 at lysine 4 (H3K4me3). The importance of menin-dependent H3K4me3 in normal and transformed pancreatic endocrine cells is unclear. To study the role of menin-dependent H3K4me3, we performed in vitro differentiation of wild-type as well as menin-null mouse embryonic stem cells (mESCs) into pancreatic islet-like endocrine cells (PILECs). Gene expression analysis and genome-wide H3K4me3 ChIP-Seq profiling in wild-type and menin-null mESCs and PILECs revealed menin-dependent H3K4me3 at the imprinted Dlk1-Meg3 locus in mESCs, and all four Hox loci in differentiated PILECs. Specific and significant loss of H3K4me3 and gene expression was observed for genes within the imprinted Dlk1-Meg3 locus in menin-null mESCs and the Hox loci in menin-null PILECs. Given that the reduced expression of genes within the DLK1-MEG3 locus and the HOX loci is associated with MEN1-like sporadic tumors, our data suggests a possible role for menin-dependent H3K4me3 at these genes in the initiation and progression of sporadic pancreatic endocrine tumors. Furthermore, our investigation also demonstrates that menin-null mESCs can be differentiated in vitro into islet-like endocrine cells, underscoring the utility of menin-null mESC-derived specialized cell types for genome-wide high-throughput studies. Genome-wide mapping of H3K4me3 and microarray gene expression profiling in TC-1 wild-type (WT) mESCs, menin-null (Men1-ko) mESCs (3.2N), pancreatic islet-like endocrine cells (PILECs) derived from WT mESCs, and PILECs derived from Men1-ko mESCs.

2012-05-31 | E-GEOD-37775 | biostudies-arrayexpress

A cDNA microarray analysis was performed on HepG2 or L-02 cells with either vectors or constructs expressing MEN1

2015-07-07 | GSE70556 | GEO

Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors (ChIP-Seq)

2012-06-01 | E-GEOD-37774 | biostudies-arrayexpress