Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE29069
PROVIDER: PRJNA142889 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR201987.fastq.gz | Fastqsanger.gz | |||
| SRR201988.fastq.gz | Fastqsanger.gz | |||
| SRR201989.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 3 of 3 |
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Project description:We profiled the transcriptomes of latency-competent cells derived from the human cancer cell lines H2087 (lung adenocarcinoma) and HCC1954 (breast adenocarcinoma) in mitogen-rich and mitogen-low media (MRM and MLM, respectively). In addition, we analyzed the epigenetic landscape of these cell lines under MLM conditions. H2087 and HCC1954 parental and latency-competent cell derivatives (LCCs) were grown for 48hr in mitogen-rich or mitogen-low conditions in vitro, and whole RNA was extracted for RNA-seq profiling. Cell lines were also grown in MLM conditions and DNA extracted for ChIP-Seq experiments.
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Project description:For the purpose of characterization of the 9p24 amplicon, we carried out high-resolution array CGH (Agilent 244K chip) analysis of four cancer cell lines, including three breast cancer cell lines, Colo824, HCC1954 and HCC70, and one esophageal cancer cell line, KYSE150.
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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.
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