Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Methylomic analysis identifies epigenetically silenced genes and implies an activation of β-catenin signal in cervical cancer

ABSTRACT: Using the pools of DNA from squamous cervical carcinomas (SCC) and DNA from normal scraping cells discovered the abnormal changes of genomic wide methylation by methylation BeadChip. The 61 genes were selected to validate by quantitative methylation specific PCR (qMSP) and bisulfite pyrosequencing in further processes. A CpG islands methylator phenotype (CIMP) was confirmed at 14 candidates in an independent set contained a spectrum of scraping cells form abnormal cervical lesions. In addition, we found among of 7 genes were announced to imply to potentially biological functions of β-catenin signal.

ORGANISM(S): Homo sapiens

PROVIDER: GSE47351 | GEO | 2014/06/26

SECONDARY ACCESSION(S): PRJNA205245

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Methylomic analysis identifies epigenetically silenced genes and implies an activation of β-catenin signal in cervical cancer

Project description:Using the pools of DNA from squamous cervical carcinomas (SCC) and DNA from normal scraping cells discovered the abnormal changes of genomic wide methylation by methylation BeadChip. The 61 genes were selected to validate by quantitative methylation specific PCR (qMSP) and bisulfite pyrosequencing in further processes. A CpG islands methylator phenotype (CIMP) was confirmed at 14 candidates in an independent set contained a spectrum of scraping cells form abnormal cervical lesions. In addition, we found among of 7 genes were announced to imply to potentially biological functions of β-catenin signal. A pool DNA collected from equal amount of DNA of 38 SCC, and the other pool collected from equal amount of DNA of 19 normal cervical scraping cells. Based on 40 percent of different methylation in two pools of samples, we selected 91 genes showed abnormal methylation in SCC. After the confirmation of gene restored expression in cervical cell lines, there 61 genes showed upregulation in the treatment with demethylating drug. In addition, gel based of MSP were contributed to confirm in a small size of samples, and quantitative MSP was contributed to validated in an independent set. The methylation status of qMSP was also confirmed by bisulfite pyrosequence. Finally, we selected 14 genes demonstrated clinical relevance in the high methylation of CIMP associated to a risk factor in cervical intraepithelial neoplasia grade 3 (CIN3) and worse lesions. isk factor in cervical intraepithelial neoplasia grade 3 (CIN3) and worse lesions.

2014-06-26 | E-GEOD-47351 | biostudies-arrayexpress

Identification and functional analysis of epigenetically silenced microRNAs in colorectal cancer cells

Project description:Abnormal miRNA expression has been linked to the development and progression of human cancers, and such dysregulation can result from aberrant DNA methylation. We combined the analysis of miRNA expression data deposited with empirical DNA methylation data in HCT116 and DKO colon cancer cells (SRA accession# SRP001414) to identify novel DNA methylation regulated miRNAs. ABSTRACT: Abnormal microRNA (miRNA) expression has been linked to the development and progression of several human cancers, and such dysregulation can result from aberrant DNA methylation. While a small number of miRNAs is known to be regulated by DNA methylation, we postulated that such epigenetic regulation is more prevalent. By combining MBD-isolated Genome Sequencing (MiGS) to evaluate genome-wide DNA methylation patterns and microarray analysis to determine miRNA expression levels, we systematically searched for candidate miRNAs regulated by DNA methylation in colorectal cancer cell lines. We found 64 miRNAs to be robustly methylated in HCT116 cells and/or DNMT-1 and 3B doubleknock cells (DKO); eighteen of them were located in imprinting regions or already reported to be regulated by DNA methylation. In the remaining 46 miRNAs, expression levels of 18 were consistent with their DNA methylation status. Finally, 10 miRNAs were up-regulated by 5-aza-2'-deoxycytidine treatment and identified to be novel miRNAs regulated by DNA methylation. Moreover, we demonstrated the functional relevance of these epigenetically silenced miRNAs by ectopically expressing select candidates, which resulted in inhibition of growth and migration of cancer cells. Our study also provides a reliable strategy to identify DNA methylation-regulated miRNAs by combining DNA methylation profiles and expression data. [miRNA expression]: Total RNA was extracted from 3 biological replicate sets of HCT116 and DMNT-1 and 3B double knock out HCT116 (DKO) colorectal cancer cells.

2011-05-20 | E-GEOD-26819 | biostudies-arrayexpress

Breast Cancer Methylomes Establish an Epigenomic Foundation for Metastasis

Project description:Cancer-specific changes in DNA methylation can alter genetic stability, genomic structure, and gene expression. Promoter CpG island methylation can result in transcriptional silencing and plays an important role in the oncogenic process. We used genome-wide analysis to characterize the methylomes of breast cancers with diverse metastatic behavior. Here, we describe the identification of novel groups of breast tumors characterized by the presence or absence of coordinate hypermethylation at a large number of genes, demonstrating the existence of a breast-CpG island methylator phenotype (B-CIMP). B-CIMP imparts a distinct epigenomic profile and is a strong determinant of metastatic potential. Gene Expression Samples (GSM647057-GSM647077): Twenty-one breast cancer primary samples were analyzed. There are 10 CIMP positive and 11 CIMP negative samples. Methylation Profiling Samples (GSM651372-GSM651410): Thirty-nine breast cancer primary samples were analyzed. There are 17 CIMP positive and 22 CIMP negative samples.

2011-03-31 | E-GEOD-26349 | biostudies-arrayexpress

DNA methylation instability by BRAF-mediated TET silencing and lifestyle-exposure divides colon cancer pathways [BrafV637E knock-in ]

Project description:Promoter hypermethylation divides colon cancers into subtypes with and without a CpG island methylator phenotype (CIMP). Here, we performed genome-wide DNA methylation profiling of colonic normal and tumor tissues to dissect development of CpG hypermethylation in colon carcinogenesis. This identified age-environment related versus genetically driven CpG hypermethylation, the latter being associated with CIMP cancers. We found a strong association between BRAFV600E mutation and downregulation of the DNA demethylases TET1 and TET2. Expression of BRAFV600E in CIMP cancer cells suppressed TET1 transcription, which was sufficient to establish hypermethylation at CIMP genes promoters, including that of TET2. This phenotype was reverted by the BRAFV600E inhibitor vemurafenib. Thus, BRAFV600E, via impairment of cytosine de-methylation, is a genetic driver of CIMP in colon tumorigenesis.

2019-12-18 | GSE108606 | GEO

DNA methylation instability by BRAF-mediated TET silencing and lifestyle-exposure divides colon cancer pathways [Colo320 cell line]

2019-12-18 | GSE124915 | GEO

DNA methylation instability by BRAF-mediated TET silencing and lifestyle-exposure divides colon cancer pathways [Caco2 cell line]

2019-12-18 | GSE98533 | GEO

DNA methylation instability by BRAF-mediated TET silencing and lifestyle-exposure divides colon cancer pathways [3 cell lines]

2019-12-18 | GSE98532 | GEO

Transcriptomic and epigenetic analyses of mouse organoids expressing BrafV600E mutation [Exome-seq]

Project description:Abnormal promoter DNA hypermethylation arises early during tumorigenesis and yet its role in cancer initiation has remained underexplored. An important scenario for examining this is, BRAFV600E-mutant colon adenocarcinomas (COAD) which most often arise in the proximal colon and harbor extensive, abnormal gene promoter CpG-island methylation or the methylator phenotype (CIMP). How CIMP and BRAF-mutations specifically interact for COAD initiation has remained unclear. Using mouse colon-derived organoids, we show promoter hypermethylation spontaneously arises in wild type cells mimicking “aging like” phenotype. The silenced genes sufficiently activate the Wnt pathway, causing a stem–like state and profound differentiation block. This phenotype renders long-term cultured organoids to be rapidly susceptible to transformation by BRAFV600E with features of typical right-sided COAD. Our studies tightly link epigenetic abnormalities, suggested to arise with aging, to intestinal cell fate changes and define an “epi-driver” role for multiple abnormally silenced genes that predispose to BRAFV600E-driven colon tumorigenesis.

2019-01-01 | GSE121672 | GEO

Trancriptomic and epigenetic analyses of mouse organoids expressing BrafV600E mutation [BiSulfite-seq]

2019-01-01 | GSE120759 | GEO

Trancriptomic and epigenetic analyses of mouse organoids expressing BrafV600E mutation [array]

2019-01-01 | GSE114800 | GEO