Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide methylation analysis of AOM/DSS-induced colon tumors

ABSTRACT: Genome-wide methylation analysis was performed by methylated DNA immunoprecipitation (MeDIP)-CpG island (CGI) microarray analysis to identify candidate CGIs specifically methylated in mouse colon tumors associated with colitis. We sucessfully identified 23 candidate CGIs methylated in tumors. Two samples were analyzed by MeDIP-CGI microarray. One is a pool of two AOM/DSS-induced colon tumors in BALB/c mice and another is a pool of two normal colonic epithelial cell samples obtained from untreated BALB/c mice by the crypt isolation technique. The pool of normal colonic epithelial cell samples was used as reference. Dye-swaps were not perfromed. The methylation statuses of CGIs identified by microarray were confirmed by another method, methylation-specific PCR.

ORGANISM(S): Mus musculus

SUBMITTER: Satoshi Yamashita

PROVIDER: E-GEOD-21333 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Genome-wide methylation analysis of AOM/DSS-induced colon tumors

Project description:Genome-wide methylation analysis was performed by methylated DNA immunoprecipitation (MeDIP)-CpG island (CGI) microarray analysis to identify candidate CGIs specifically methylated in mouse colon tumors associated with colitis. We sucessfully identified 23 candidate CGIs methylated in tumors.

2011-06-30 | GSE21333 | GEO

BANP is an essential transcription factor that opens chromatin and activates CpG island regulated genes

Project description:While the majority of RNA polymerase II initiation events in mammalian genomes take place within CpG island (CGI) promoters, our understanding of their regulation remains limited. Here we combine single-molecule footprinting with interaction proteomics to identify BANP as a critical CGI regulator and the long sought-after TF that binds the orphan CGCG element in mouse and human. We show that BANP drives the activity of essential metabolic genes in the mouse genome in pluripotent and terminally differentiated cells. However, BANP binding is strongly repelled by DNA methylation of its motif in vitro and in vivo, which epigenetically restricts most binding to CGIs and accounts for its absence at aberrantly methylated CGIs in cancer cells. Upon binding to an unmethylated motif, BANP opens chromatin and phases nucleosomes. Our results establish Banp as a critical activator and put forth a model whereby CGI promoter activity relies on methylation-sensitive TFs capable of chromatin opening.

2021-06-16 | PXD024794 | Pride

Genome-wide methylation analysis of esophageal squamous cell carcinoma

Project description:Genome-wide methylation analysis was performed by methylated DNA immunoprecipitation-CGI microarray analysis. A pool of four cancer samples without lymph node metastasis, two pools of four cancer samples with lymph node metastasis, and three metastatic lymph nodes were prepared from the patients, and analyzed by MeDIP-CGI microarray.

2010-12-21 | E-GEOD-21238 | biostudies-arrayexpress

Read-through transcription as a general mechanism mediating methylation and silencing of intragenic CGIs [small RNA-seq]

Project description:The human genome contains approximately 27,700 CpG islands (CGIs). Most are associated with promoters and their DNA is nearly always unmethylated. By contrast, CGIs lying within the bodies of genes usually become methylated during differentiation and development. CGIs also normally become methylated at X-inactivated and imprinted genes and abnormally methylated in genome rearrangements and in malignancy. In such circumstances, methylation of CGIs is often associated with RNA transcripts reading through these elements but the relationship of this RNA to methylation of CGIs is not clear. Here we investigated a previously described form of α-thalassemia caused by a genome rearrangement leading to abnormal transcription and DNA methylation of the CGI at the promoter of the α-globin gene. We show that transcription per se is responsible for DNMT3B-mediated methylation of the globin CGI, and that this is a general mechanism responsible for methylation of most intragenic CpG islands.

2017-08-10 | GSE84354 | GEO

Read-through transcription as a general mechanism mediating methylation and silencing of intragenic CGIs [CAP-Seq]

2017-08-10 | GSE84353 | GEO

Read-through transcription as a general mechanism mediating methylation and silencing of intragenic CGIs [H3K36me3_ChIP-seq]

2017-08-10 | GSE84352 | GEO

The presence of RNA polymerase II, active or stalled, predicts epigenetic fate of promoter CpG islands.

Project description:Instructive mechanisms are present for induction of DNA methylation, as shown by methylation of specific CpG islands (CGIs) by specific inducers and in specific cancers. However, instructive factors involved are poorly understood, except for involvement of low transcription and trimethylation of histone H3 lysine 27 (H3K27me3). Here, we used methylated DNA immunoprecipitation (MeDIP) combined with a CGI oligonucleotide microarray analysis, and identified 5510 and 521 genes with promoter CGIs resistant and susceptible, respectively, to DNA methylation in prostate cancer cell lines. Expression analysis revealed that the susceptible genes had low transcription in a normal prostatic epithelial cell line. Chromatin immunoprecipitation with microarray hybridization (CHiP-chip) analysis of RNA polymerase II (Pol II) and histone modifications showed that, even among the genes with low transcription, the presence of Pol II was associated with marked resistance to DNA methylation (OR = 0.22; 95% CI = 0.12-0.38), and H3K27me3 was associated with increased susceptibility (OR = 11.20; 95% CI = 7.14-17.55). The same was true in normal human mammary epithelial cells for 5430 and 733 genes resistant and susceptible, respectively, to DNA methylation in breast cancer cell lines. These results showed that the presence of Pol II, active or stalled, and H3K27me3 can predict the epigenetic fate of promoter CGIs independently of transcription levels. To analyze DNA methylation status in normal and cancer cells, MeDIP-CGI oligonucleotide microarray analysis was performed. To analyze expression and histone modification status in normal cells, GeneChip analysis and ChIP-oligonucleotide microarray analysis were performed.

2010-05-15 | E-GEOD-15154 | biostudies-arrayexpress

Cell Type-Specific DNA Methylation at Intragenic CpG Islands in the Immune System (MAP-Seq and ChIP-Seq data)

Project description:Human and mouse genomes contain a similar number of CpG islands (CGIs), which are discrete CpG-rich DNA sequences associated with transcription start sites. In both species, about 50% of all CGIs are remote from annotated promoters, but nevertheless often have promoter-like features. To document the role of CGI methylation in cell differentiation, we analysed DNA methylation at a comprehensive CGI set in cells of the mouse hematopoietic lineage. Using a method that potentially detects ~33% of genomic CpGs in the methylated state (>7 million) we found that large differences in gene expression were accompanied by surprisingly few DNA methylation changes. There were, however, many DNA methylation differences between hematopoietic cells and a distantly related tissue, brain. Altered DNA methylation occurred predominantly at CGIs within gene bodies, which have the properties of cell type-restricted promoters, but infrequently at annotated gene promoters or CGI flanking sequences. Elevated intragenic CGI methylation correlated with silencing of the associated gene. Differentially methylated intragenic CGIs tended to lack H3K4me3 and associate with a transcriptionally repressive environment regardless of methylation state. Our results indicate that DNA methylation changes play a relatively minor role in the late stages of differentiation, but point to a distinct role for intragenic CGIs.

2011-05-23 | GSE25688 | GEO

Cell Type-Specific DNA Methylation at Intragenic CpG Islands in the Immune System (gene expression data)

2011-05-23 | GSE25578 | GEO

Cell Type-Specific DNA Methylation at Intragenic CpG Islands in the Immune System (MAP-Seq and ChIP-Seq data)

2011-05-23 | E-GEOD-25688 | biostudies-arrayexpress