This SuperSeries is composed of the SubSeries listed below.
Relationship between gene body DNA methylation and intragenic H3K9me3 and H3K36me3 chromatin marks.
Specimen part, Cell line
View SamplesThis is one of expressional parts of the study. These data were correlated to epigenetic marks and CG density of genes in analyzed cells. The whole study has a following summary: To elucidate possible roles of DNA methylation and chromatin marks in transcription, we performed epigenetic profiling of chromosome 19 in human bronchial epithelial cells (HBEC) and in the colorectal cancer cell line HCT116 as well as its counterpart with double knockout of DNMT1 and DNMT3B (HCT116-DKO). We found that H3K9me3 forms intragenic chromatin blocks along genes with low CpG density in the gene body. Analysis of H3K36me3 profiles indicated that this mark associates either with active genes with low CpG density and H3K9me3 in the gene body or with active genes with high CpG density and DNA hypermethylation in the gene body. In HCT116 cells with double knockout of DNMT1 and DNMT3B, transcription of genes with low CpG density in the gene body was highly elevated and associated with promoter DNA demethylation and rearrangement of H3K9me3 and H3K36me3 occupation. Our finding suggests that similar to DNA methylation, H3K9me3 may play a role in intragenic gene regulation. Further, we observed that a combination of low CpG density in gene bodies together with H3K9me3 and H3K36me3 marking is a specific epigenetic feature of zinc finger (ZNF) genes, which comprise 90% of all genes carrying both histone marks on chromosome 19. For high CpG density genes, transcription and H3K36me3 occupancy were not changed in condition of partial or intensive loss of DNA methylation in gene bodies in the HCT116-DKO cell line. siRNA experiments with SETD2 knockdown in both HBEC and HCT116-DKO cell lines failed to reduce DNA methylation in gene bodies under conditions of H3K36me3 depletion. Our study suggests that the H3K36me3 and DNA methylation marks in gene bodies are established independently from each other and points to similar functional roles of intragenic DNA methylation and intragenic H3K9me3 for CpG-rich and CpG-poor genes, respectively.
Relationship between gene body DNA methylation and intragenic H3K9me3 and H3K36me3 chromatin marks.
Specimen part, Cell line
View SamplesGene expression data from AML cell lines, MOLM-14, U937, THP-1 and HL-60, that were infected with a scrambled control hairpin (shControl), two shRNAs directed against GSK-3B (shGSK3B_1 and shGSK3B_2), or two shRNAs directed against GSK-3A (shGSK3A_5 and shGSK3A_6).
The intersection of genetic and chemical genomic screens identifies GSK-3α as a target in human acute myeloid leukemia.
Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Loss of the polycomb mark from bivalent promoters leads to activation of cancer-promoting genes in colorectal tumors.
Specimen part, Disease, Subject
View SamplesAnalysis of expression changes between colon tumors (Duke's stage II) and matching colon mucosa tissues using Affymetrix GeneChip Human Gene 2.0 ST arrays.
Loss of the polycomb mark from bivalent promoters leads to activation of cancer-promoting genes in colorectal tumors.
Specimen part, Disease, Subject
View SamplesIn this study, we used Global Run-On sequencing (GRO-seq), a method that assays the genome-wide location and orientation of all active RNA polymerases. We generated a global profile of active transcription at ERa binding sites in MCF-7 human breast cancer cells in response to short time course of E2 treatment. This method enabled us to detect active transcription at enhancers and define a class of primary transcripts transcribed uni- or bidirectionally from the ERa binding sites. The raw data used in this study is from GSE27463 but sequenced to a greater depth. Overall design: Using GRO-seq over a time course (0, 10, 40 min) of estrogen signaling in ER-alpha positive MCF-7 human breast cancer cells.
Enhancer transcripts mark active estrogen receptor binding sites.
Cell line, Treatment, Subject
View SamplesInhibiton of NSD2 by shRNA induces K562 differentiation via increasing erythroid specfic lineage factors
Proteosomal degradation of NSD2 by BRCA1 promotes leukemia cell differentiation.
Cell line
View SamplesKeloids are scars that extend beyond original wounds and are resistant to treatment. In order to improve understanding of the molecular basis of keloid scarring, we have assessed the genomic profiles of keloid fibroblasts and keratinocytes.
Keloid-derived keratinocytes exhibit an abnormal gene expression profile consistent with a distinct causal role in keloid pathology.
Sex, Age, Specimen part, Race
View SamplesRNA Pol II transcription has been implied to be either regulated by the general transcription factor TFIID or the co-activator SAGA. Also, this dominancy of either SAGA or TFIID might be according to the existance, or not, of a TATA consensus sequence.
Transcription of Nearly All Yeast RNA Polymerase II-Transcribed Genes Is Dependent on Transcription Factor TFIID.
Treatment
View SamplesThe concept of age-dependent host control of cancer development raises the natural question of how these effects manifest across the host tissue/organ types with which a tumor interacts, one important component of which is the aging immune system. To investigate this, changes in the spleen, an immune nexus in the mouse, was examined for its age-dependent interactive influence on the carcinogenesis process. The model is the C57BL/6 male mice (adolescent, young adult, middle-aged, and old or 68, 143, 551 and 736 days old respectively) with and without a syngeneic murine tumor implant. Through global transcriptome analysis, immune-related functions were found to be key regulators in the spleen associated with tumor progression as a function of age with CD2, CD3, CCL19, and CCL5 being the key molecules involved. Surprisingly, other than CCL5, all key factors and immune-related functions were not active in spleens from non-tumor bearing old mice. Our findings of age-dependent tumor-spleen signaling interaction suggest the existence of a global role of the aging host in carcinogenesis. Suggested is a new avenue for therapeutic improvement that capitalizes on the pervasive role of host aging in dictating the course of this disease.
Tumor-host signaling interaction reveals a systemic, age-dependent splenic immune influence on tumor development.
Sex, Age, Specimen part, Disease, Disease stage
View Samples