Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

ChIP-Seq for RNA Polymerase II in MCF7 breast cancer cells

ABSTRACT: Enrichment PolII binding at TSS and gene body is an indication of active transcription. The genome-wide PolII occupancy was determined using ChIP-Seq in MCF7. ChIP was performed using an antibody against total RNA PolII (ab5408-100; Abcam). ChIP DNA and input DNA were sequenced with an Illumina HiSeq 2000 instrument.

INSTRUMENT(S): Illumina HiSeq 2000

ORGANISM(S): Homo sapiens

SUBMITTER: Ming-Ta Hsu

PROVIDER: E-MTAB-1952 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Hierarchical clustering of breast cancer methylomes revealed differentially methylated and expressed breast cancer genes.

Lin I-Hsuan IH Chen Dow-Tien DT Chang Yi-Feng YF Lee Yu-Ling YL Su Chia-Hsin CH Cheng Ching C Tsai Yi-Chien YC Ng Swee-Chuan SC Chen Hsiao-Tan HT Lee Mei-Chen MC Chen Hong-Wei HW Suen Shih-Hui SH Chen Yu-Cheng YC Liu Tze-Tze TT Chang Chuan-Hsiung CH Hsu Ming-Ta MT

PloS one 20150223 2

Oncogenic transformation of normal cells often involves epigenetic alterations, including histone modification and DNA methylation. We conducted whole-genome bisulfite sequencing to determine the DNA methylomes of normal breast, fibroadenoma, invasive ductal carcinomas and MCF7. The emergence, disappearance, expansion and contraction of kilobase-sized hypomethylated regions (HMRs) and the hypomethylation of the megabase-sized partially methylated domains (PMDs) are the major forms of methylation ...[more]

PMID: 25706888

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Project description:To advance understanding of mechanisms leading to biological and transcriptional endpoints related to estrogen action in the mouse uterus, we have mapped ERM-NM-1 and RNA polymerase II binding sites using chromatin immunoprecipitation (ChIP) followed by sequencing of enriched chromatin fragments (ChIP-seq). In the absence of hormone, 5184 ERM-NM-1 binding sites were apparent in the vehicle treated ovariectomized uterine chromatin, while 17240 were seen one hour after estrogen (E2) treatment, indicating that some sites are occupied by unliganded ERM-NM-1, and that ERM-NM-1 binding is increased by E2. Approximately 15% of the uterine ERM-NM-1 binding sites were adjacent to (<10 KB) annotated transcription start sites and many sites are found within genes or are found more than 100 KB distal from mapped genes; however, the density (sites per bp) of ERM-NM-1 binding sites is significantly greater adjacent to promoters. An increase in quantity of sites but no significant positional differences were seen between vehicle and E2 treated samples in the overall locations of ERM-NM-1 binding sites either distal from, adjacent to or within genes. Analysis of the PolII data revealed the presence of poised promoter proximal PolII on some highly upregulated genes. Additionally, co-recruitment of PolII and ERM-NM-1 to some distal enhancer regions was observed. A de novo motif analysis of sequences in the ERM-NM-1 bound chromatin confirmed that estrogen response elements (EREs) were significantly enriched. Interestingly, in areas of ERM-NM-1 binding without predicted ERE motifs, homeodomain transcription factor (Hox) binding motifs were significantly enriched. The integration of the ERM-NM-1 and PolII binding sites from our uterine ChIP-seq data with transcriptional responses revealed in our uterine microarrays has the potential to greatly enhance our understanding of mechanisms governing estrogen response in uterine and other estrogen target tissues. one sample each, vehicle ER-alpha ChIP seq,1 hour estradiol ER-alpha ChIP seq, vehicle RNA polymerase II ChIP seq,1 hour estradiol RNA polymerase II ChIP seq, input DNA

Dataset Information

ChIP-Seq for RNA Polymerase II in MCF7 breast cancer cells

Publications

Hierarchical clustering of breast cancer methylomes revealed differentially methylated and expressed breast cancer genes.

Similar Datasets

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