Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE29069
PROVIDER: PRJNA142895 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR201990.fastq.gz | Fastqsanger.gz | |||
| SRR201991.fastq.gz | Fastqsanger.gz | |||
| SRR201992.fastq.gz | Fastqsanger.gz | |||
| SRR201993.fastq.gz | Fastqsanger.gz | |||
| SRR201994.fastq.gz | Fastqsanger.gz |
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Project description:Gene expression analysis of breast cancer (HCC1954) and normal breast cells (HMEC)
| PRJNA142887 | ENA
Project description:While genetic mutation is a hallmark of cancer, many cancers also acquire epigenetic alterations during tumorigenesis including aberrant DNA hypermethylation of tumor suppressors as well as changes in chromatin modifications as caused by genetic mutations of the chromatin-modifying machinery. However, the extent of epigenetic alterations in cancer cells has not been fully characterized. Here, we describe the first complete methylome maps at single nucleotide resolution of a low-passage breast cancer cell line and primary human mammary epithelial cells. We find widespread DNA hypomethylation in the cancer cell, primarily at partially methylated domains (PMDs) in normal breast cells. Unexpectedly, genes within these regions are largely silenced in cancer cells. The loss of DNA methylation in these regions is accompanied by formation of repressive chromatin, with a significant fraction displaying allelic DNA methylation where one allele is DNA methylated while the other allele is occupied by histone modifications H3K9me3 or H3K27me3. Our results show a mutually exclusive and complementary relationship between DNA methylation and H3K9me3 or H3K27me3. These results suggest that global DNA hypomethylation in breast cancer is tightly linked to the formation of repressive chromatin domains and gene silencing, thus identifying a potential epigenetic pathway for gene regulation in cancer cells and suggesting a possible new approach toward the development of cancer therapeutics. mRNA-Seq of polyA-selected RNA from breast cancer HCC1954 and normal breast HMEC. 36 cycles of sequencing on Illumina platform.
2011-09-16 | E-GEOD-29119 | biostudies-arrayexpress
Project description:Background: Epigenetic modification is a hallmark of cancer cells achieved through altered patterns of DNA methylation, histone modifications and nucleosome positions. These events have only been described in detail at gene promoters. Results: Here, we integrate multiple epigenome-wide maps to evaluate the scope of global epigenetic reprogramming in cancer cells at enhancers and insulators. Using high-resolution simultaneous mapping of global DNA methylation and nucleosome positions within individual DNA strands (NOMe-Seq), we observe a reorganization of the DNA methylome coupled with simultaneous modulation of nucleosome depleted regions (NDRs) at distal regulatory elements in cancer cells. We show that while NDRs are preferentially found at enhancers in normal breast and prostate epithelial cells, there are fewer NDRs coupled with increased DNA methylation detected at enhancersin cancer cells. Our data suggests that the acquisition of a nucleosome is key to DNA hypermethylation susceptibility and contributes to epigenetic silencing of enhancers in cancer, which can notably occur without loss of H3K4me1. Further we observe that NDRs are not necessary for peripheral phasing of adjacent nucleosomes, contrary to the common dogma, and show that nucleosomes remain organized and phased, even in the absence of a NDR as an anchor. Finally we observe the potential for transcription factors (TF) to organize NDRs genome-wide; all TF-binding sites are strongly hypomethylated and some show extensive peripheral nucleosome phasing. Conclusion: Together our findings suggest that, in addition to epigenetic alterations to promoter regions in cancer, there is substantial disruption to the distal regulatory architecture that provides an additional layer of epigenetic plasticity in malignancy. NOMe-seq, ChIP-seq for 5 marks and input control for breast normal (HMEC), breast cancer (MCF7), prostate normal (PrEC) and prostate cancer (PC3) cell lines
2014-06-04 | E-GEOD-57498 | biostudies-arrayexpress
Project description:Aberrant DNA methylation is frequently observed in cancer. The aim of the study was to determine how is DNA methylation of miRNA genes changed in breast cancer cell lines an breast tumor specimens. Breast cancer cell lines vs. HMEC. Breast tumor tissue specimens vs. non-tumor tissue specimens. Biological replicates: 12 breast tumor specimens, 5 breast non-tumor specimens, 7 breast cancer cell lines, 3 HMEC genotypes, 3 HMF genotypes. Immunoprecipitation using anti-Methylcytosine (5MeC) antibody.
2012-05-25 | E-GEOD-38254 | biostudies-arrayexpress
Project description:DNA methylation of prostatic normal cells (PrEC), normal mammary epithelial cells (HMEC), prostate cancer cell line (MDA-PCa-2b), and breast cancer cell lines (BT474 and MDA-MB-231) was analyzed by MeDIP-on-chip analysis. DNA obtained from each cells was immunoprecipitated by anti 5-methylcytidine antibody. IP DNA and input DNA were labeled with Cy5 and Cy3, respectively, and then analyzed by using human CpG island microarray provided by Agilent Technologies.
2011-06-06 | E-GEOD-28284 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of normal and breast cancer samples. The Illumina Infinium 450k Human DNA methylation Beadchip v1.1 was used to obtain DNA methylation profiles across approximately 485577 CpGs in breast cancer and normal samples. Samples included 40 normal, 80 breast cancer samples.
2015-03-11 | GSE66695 | GEO
Project description:Genome-wide location analysis in breast cancer cells (HCC1954)
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Project description:While genetic mutation is a hallmark of cancer, many cancers also acquire epigenetic alterations during tumorigenesis including aberrant DNA hypermethylation of tumor suppressors as well as changes in chromatin modifications as caused by genetic mutations of the chromatin-modifying machinery. However, the extent of epigenetic alterations in cancer cells has not been fully characterized. Here, we describe the first complete methylome maps at single nucleotide resolution of a low-passage breast cancer cell line and primary human mammary epithelial cells. We find widespread DNA hypomethylation in the cancer cell, primarily at partially methylated domains (PMDs) in normal breast cells. Unexpectedly, genes within these regions are largely silenced in cancer cells. The loss of DNA methylation in these regions is accompanied by formation of repressive chromatin, with a significant fraction displaying allelic DNA methylation where one allele is DNA methylated while the other allele is occupied by histone modifications H3K9me3 or H3K27me3. Our results show a mutually exclusive and complementary relationship between DNA methylation and H3K9me3 or H3K27me3. These results suggest that global DNA hypomethylation in breast cancer is tightly linked to the formation of repressive chromatin domains and gene silencing, thus identifying a potential epigenetic pathway for gene regulation in cancer cells and suggesting a possible new approach toward the development of cancer therapeutics. ChIP-methylC-Seq on H3K9me3, H3K27me3, and H3K36me3 in breast cancer HCC1954. 36 cycles of sequencing on Illumina platform.
2011-09-16 | E-GEOD-29120 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of normal breast, normal adjacent and breast cancer tissue
| PRJNA287264 | ENA
Project description:Genome wide DNA methylation profiling of normal and breast cancer samples. The Illumina Infinium 450k Human DNA methylation Beadchip v1.1 was used to obtain DNA methylation profiles across approximately 485577 CpGs in breast cancer and normal samples. Samples included 40 normal, 80 breast cancer samples. Bisulphite converted DNA from the 120 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip v1.1
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