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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

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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

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Breast Cancer Methylomes Establish an Epigenomic Foundation for Metastasis

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

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.

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