The methylome of Alu repeats in colon cancer (NSUMA)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Miguel Peinado
PROVIDER: E-GEOD-72749 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Next Generation Sequencing of Unmethylated Alu (NSUMA) interrogation of more than 130,000 individual Alus for differential methylation with concomitant analysis of copy number variations applied to the study of hypomethylation in primates. 3 replicates of Gorilla gorilla, Pan troglodytes, Pongo pygmaeus and Homo sapiens were studied.
2015-09-10 | E-GEOD-72877 | biostudies-arrayexpress
Project description:A large-scale characterization of the methylation states of candidate CpG islands (CGIs) throughout the gastric cancer methylome has not previously been conducted. Genome-wide DNA methylation profiles were compared between 4 metastatic and 4 non-metastatic gastric carcinomas (GCs) and their surgical margins (SMs). The GC genome showed significantly higher proportions of hypomethylation in the promoter and exon-1 regions, as well as increased hypermethylation of intragenic fragments when compared to SMs. Differential methylation was observed in CGIs near transcription start sites of 546 genes between GCs and SMs, and 601 genes between metastatic and non-metastatic GCs. From the list of differentially methylated CGIs, 68 candidate genes and 10 known tumor-related genes were selected for further characterization based on their known molecular function using DHPLC. Significant differential methylation was validated in the CGIs of 15 genes between GCs and SMs (Ps<0.05) and confirmed using bisulfite-sequencing. These genes include BMP3, BNIP3, CDKN2A, ECEL1, ELK1, GFRA1, HOXD10, KCNH1, PSMD10, PTPRT, SIGIRR, SRF, TBX5, TFPI2, and ZNF382. Hypomethylation of CGIs correlated with up-regulation of GFRA1 expression in GCs, while hypermethylation of other genes inactivated their transcription. Most importantly, prevalence of GFRA1, SRF, and ZNF382 methylation alterations were inversely and coordinately associated with GC metastasis and the patients’ overall survival throughout discovery and testing cohorts in China as well as independent validation cohorts in Japan and Korea. In conclusion, methylation changes in the CGIs of 15 genes correlated strongly with GC development. GFRA1 hypomethylation and SRF and ZNF382 hypermethylation are potential synergistic biomarkers for the prediction of GC metastasis. To identify differential methylation of CGIs related to GC development and metastasis, genome-wide DNA methylation changes in 8 pairs of GC and SM samples were analysed using the MCAM assay with a 99K custom-designed Agilent oligonucleotide microarray composed of 99,027 probes targeting 6,177 unique protein-coding genes containing at least two methylation-sensitive/insensitive SmaI/ XmaI restriction sites (CCC|GGG/ C|CmCGGG) as described in Shen et al, PLoS Genet 3, 2023-2036 (2007).
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Project description:To examine methylation profile of the CpG promoters in glioma stem cells
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Project description:Polycomb repressive complexes (PRC) are frequently implicated in human cancer acting either as oncogenes or tumor suppressors. Here we show that PRC2 is a critical regulator of Kras-driven non-small-cell lung cancer (NSCLC) progression. Modulation of PRC2 by either Ezh2 overexpression or Eed deletion enhances Kras-driven adenomagenesis and inflammation, respectively. Eed-loss-driven inflammation leads to massive macrophage recruitment and marked decline in tissue function. Additional Trp53 inactivation activates a cell autonomous epithelial-to-mesenchymal transition (EMT) program leading to an invasive mucinous adenocarcinoma. A switch between methylated/acetylated chromatin underlies the tumor phenotypic evolution, prominently involving genes controlled by Hippo/Wnt-signaling. Our observations in the mouse models were conserved in human cells. Importantly, PRC2 inactivation results in context-dependent phenotypic alterations, with implications for its therapeutic application. We generated ChIP-seq from primary Kras;p53 (KP) cells in culture with and without Eed (KPE) and from KP primary tumors generated by injection of NSCLC into the tail vein. Mice were sacrificed on the onset of shortness of breath. We generated genome-wide expression profiles (RNA-seq) and Nuclease Accessibility (NA)-seq in primary KP and KPE tumor cells. NA-seq was also performed in A549 cells.
2016-01-15 | E-GEOD-61190 | biostudies-arrayexpress
Project description:Cytosine methylation of DNA is an evolutionarily conserved mechanism from plants to animals with crucial roles in gene regulation. However, the variation between methylomes of normal tissues is largely unexplored. To better understand the epigenetic variation of a normal individual, we profiled DNA methylation using whole genome bisulfite sequencing in 17 tissues isolated from an individual mouse. We observed a unique distribution of CpG methylation for each tissue, which cluster based on cell lineage. Global analysis identified only one-eighth of the genome as tissue-specifically methylated. Remarkably, the vast majority of these regions exhibit hallmarks of cis-regulatory activity. Our results also reveal a novel class of dormant enhancers in adult tissues which retain an epigenetic memory of regulatory elements active during development. Together, these results expand the repertoire of regulatory information encoded within the methylome, and suggest mapping it as an alternative method to identify cell-type specific regulatory elements. whole genome bisulfite sequencing of mouse adult tissue
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