Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA391164 | ENA |
REPOSITORIES: ENA
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Project description:We performed ChIP-seq for histone modifications to map chromatin status and dynamics during MCF10A-ER-Src cell transformation.
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Project description:We performed DNase-seq to study the dynamic genome-wide chromatin accessibility during MCF10A-ER-Src cell transformation.
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Project description:siSTAT3 knockdown of a tamoxifen initiated, transformation inducible, breast cancer model system (MCF10A-ER-Src), with associated controls of EtOH and siNEG treatments. A description of MCF10A-ER-Src cells can be found here: www.encodeproject.org
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Project description:Ribosome profiling and RNA sequencing of MCF10A-ER-Src and fibroblast cell transformation
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Project description:We applied ribosome profiling and RNA sequencing to examine gene expression regulation during oncogenic cell transformation. One model involves normal mammary epithelial cells (MCF10A) containing ER-Src. Treatment of such cells with tamoxifen rapidly induces Src, thereby making it possible to kinetically follow the transition between normal and transformed cells. The other model consists of three isogenic cell lines derived from primary fibroblasts in a serial manner (Hahn et al., 1999). EH cell is immortalized by overexpression of telomerase (hTERT), and exhibits normal fibroblast morphology. EL cell expresses hTERT along with both large and small T antigens of Simian virus 40, and it displays an altered morphology but is not transformed. ELR cell expresses hTERT, T antigens, and an oncogenic derivative of Ras (H-RasV12).
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Project description:The onset and progression of breast cancer are linked to genetic and epigenetic changes that alter the normal programming of cells. Epigenetic modifications of DNA and histones contribute to chromatin structure that results in the activation or repression of gene expression. Several epigenetic pathways have been shown to be highly deregulated in cancer cells. Targeting specific histone modifications represents a viable strategy to prevent oncogenic transformation, tumor growth or metastasis. Methylation of histone H3 lysine 4 has been extensively studied and shown to mark genes for expression; however this residue can also be acetylated and the specific function of this alteration is less well known. To define the relative roles of histone H3 methylation (H3K4me3) and acetylation (H3K4ac) in breast cancer, we determined genomic regions enriched for both marks in normal-like (MCF10A), transformed (MCF7) and metastatic (MDA-MB-231) cells using a genome-wide ChIP-Seq approach. Our data revealed a genome-wide gain of H3K4ac associated with both early and late breast cancer cell phenotypes, while gain of H3K4me3 was predominantly associated with late stage cancer cells. Enrichment of H3K4ac was overrepresented at promoters of genes associated with cancer-related phenotypic traits, such as estrogen response and epithelial-to-mesenchymal transition pathways. Our findings highlight an important role for H3K4ac in predicting epigenetic changes associated with early stages of transformation. In addition, our data provide a valuable resource for understanding epigenetic signatures that correlate with known breast cancer-associated oncogenic pathways. RNA-Seq of cell lines MCF10A, MCF7 and MDA-MB-231.
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Project description:The molecular signature at histone H3K4me3 and H3K27me3 involved in epigenetic regulation of normal (MCF10A) and transformed (MCF7, MDA-MB-231) breast cells using ChIP-Seq technology. This study examines the dynamic distribution of H3K4me3, associated with active chromatin, and H3K27me3, associated with repressed chromatin, histone modifications to provide an understanding of the changes in epigenetic regulation associated with the unique breast cancer subtypes. histone H3K4me3 and H3K27me3 ChIP-seq normal (MCF10A) and transformed (MCF7, MDA-MB-231) breast cells Please note that the 'H3K4me3' and 'input' data are duplicated records of the samples represented in GSE69377 for the convenient retrieval of the complete raw data from SRA.
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