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

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 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE52301 | GEO | 2013/11/13

SECONDARY ACCESSION(S): PRJNA227373

REPOSITORIES: GEO

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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. Comparison of ChIP-on-chip results between tumor(C) and adjacent tissues(N) from three HCC specimens with H3K27me3

2013-11-13 | E-GEOD-52301 | biostudies-arrayexpress

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 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.

2013-11-08 | GSE52190 | GEO

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.

2015-07-07 | E-GEOD-70556 | biostudies-arrayexpress

Spatial interplay between Polycomb and Trithorax complexes controls transcriptional activity in T lymphocytes [ChIP-Seq]

Project description:Trithorax group (TrxG) and Polycomb group (PcG) proteins are two mutually antagonistic chromatin modifying complexes, however, how they together mediate transcriptional counterregulation remains unknown. Genome-wide analysis revealed that binding of Ezh2 and Menin, central members of the PcG and TrxG complexes, respectively, were reciprocally correlated. Moreover, we identified a developmental change in the positioning of Ezh2 and Menin in differentiated T lymphocytes compared to embryonic stem cells. Ezh2-binding upstream and Menin-binding downstream of the transcription start site (TSS) was frequently found at genes with higher transcriptional levels, and Ezh2-binding downstream and Menin-binding upstream was found at genes with lower expression in T lymphocytes. Interestingly, of the Ezh2 and Menin co-occupied genes, those exhibiting occupancy at the same position displayed greatly enhanced sensitivity to loss of Ezh2. Finally, we also found that different combinations of Ezh2 and Menin occupancy were associated with expression of specific functional gene groups important for T cell development. Therefore, spatial cooperative gene regulation by the PcG and TrxG complexes may represent a novel mechanism regulating the transcriptional identity of differentiated cells.

2015-10-10 | GSE73820 | GEO

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

2015-07-07 | GSE70556 | GEO

Spatial interplay between Polycomb and Trithorax complexes controls transcriptional activity in T lymphocytes

2015-09-08 | E-GEOD-72757 | biostudies-arrayexpress

CpG Island Structure and Trithorax/Polycomb Chromatin Domains in Human Cells

Project description:TrxG and PcG complexes play key roles in the epigenetic regulation of development through H3K4me3 and H3K27me3 modification at specific sites throughout the human genome, but how these sites are selected is poorly understood. We find that in pluripotent cells, clustered CpG islands at genes predict occupancy of H3K4me3 and H3K27me3, and these "bivalent" chromatin domains precisely span the boundaries of CpG island clusters. Examination of two histone modifications (H3K4me3 and H3K27me3) in human induced pluripotent stem (hiPS) M23F cells.

2012-07-06 | E-GEOD-39137 | biostudies-arrayexpress

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)

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.

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

Menin controls the memory Th2 cell function by maintaining the epigenetic integrity of Th2 cells. [ChIP-Seq]

Project description:Post-translational modifications of histones are well-established epigenetic modifications that play an important role in gene expression and regulation. These modifications are partly mediated by the Trithorax group (TrxG) complex, which regulates the induction or maintence of gene transcription. We investigated the role of Menin, a component of the TrxG complex, in the acquisition and maintenance of T helper type 2 (Th2) cell identity using T cell-specific Menin-deficient mice. Our gene expression analysis revealed that Menin was involved in the maintenance of the high level expression of the previously identified Th2-specific genes rather than the induction of these genes. This result suggests a role of Menin in the maintenance of Th2 cell identity. Menin directly bound to the Gata3 gene locus, and this Menin-Gata3 axis appeared to form a core unit of the Th2-specific gene regulatory network. Consistent with the phenotype of Menin-deficient Th2 cells observed in vitro, Menin deficiency resulted in the attenuation of effector Th2 cell-induced airway inflammation. In addition, in memory Th2 cells, Menin was found to play an important role in the maintenance of the expression of Th2-specific genes, including Gata3, Il4, and Il13. Consequently, Menin-deficient memory Th2 cells showed an impaired abiliy to recruit eosinophils to the lung, resulting in the attenuation of memory Th2 cell-induced airway inflammation. This study confirmed the critical role of Menin in Th2 cell-mediated immune responses.

2017-05-25 | GSE99259 | GEO

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