Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

ChIP-Seq of human breast cancer cell lines treated with estrogen and tamoxifen to investigate CTCF binding

ABSTRACT: CCCTC-binding factor (CTCF) is a conserved zinc finger transcription factor involved in chromatin looping. Recent evidence has shown a role for CTCF in ER biology. This experiment maps CTCF binding genome-wide in breast cancer cells and shows that CTCF binding does not change with estrogen or tamoxifen treatment. We find a small but reproducible proportion of CTCF binding events that overlap with both the nuclear receptor estrogen receptor and the forkhead protein FoxA1. These overlapping binding events are likely to be functional as they are biased towards estrogen-regulated genes. In addition, we identify cell-line specific CTCF binding events. These cell-line specific CTCF binding events are more likely to be associated with cell-line specific ER vinding events and are also more likely to be adjacent to genes that are expressed in that particular cell line. These data suggest a positive, pro-transcriptional role for CTCF in ER-mediated gene expression in breast cancer cells.

ORGANISM(S): Homo sapiens

SUBMITTER: Gordon Brown

PROVIDER: E-MTAB-740 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

A co-ordinated interaction between CTCF and ER in breast cancer cells.

Ross-Innes Caryn S CS Brown Gordon D GD Carroll Jason S JS

BMC genomics 20111205

<h4>Background</h4>CCCTC-binding factor (CTCF) is a conserved zinc finger transcription factor that is involved in both intra- and interchromasomal looping. Recent research has shown a role for CTCF in estrogen receptor (ER) biology, at some individual loci, but a multi-context global analysis of CTCF binding and transcription activity is lacking.<h4>Results</h4>We now map CTCF binding genome wide in breast cancer cells and find that CTCF binding is unchanged in response to estrogen or tamoxifen ...[more]

PMID: 22142239

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Project description:Estrogen receptors play critical roles in both the normal physiological, and disease states of numerous tissues, including breast and uterus. Estrogen receptor alpha (ER) can activate or repress the expression of target genes upon estrogen stimulation. In order to better understand the transcriptional network of ER in breast and uterus, we generated genome wide maps ofM-BM- ER binding sites (ERBS) and gene expression profiles in breast cancer cells (MCF7 and T47D) and uterine cancer cells (ECC1 and Ishikawa) through ChIP-Seq and microarray techniques. Surprisingly, we identified large scale differences in the numbers of ERBS between these cell lines when treated with E2 (17-M-NM-2 estradiol). Besides identification of common and unique ERBS between breast and uterine cancer cell types., our data also suggest that both cell types could recruit a large set of common co-operating transcription factors (Co-TFs) and a few unique Co-TFs as well. Besides the genes that are commonly regulatedM-BM- between the different cell lines, there are a number of genes that are differentially regulated in different cell types. Gene pathway analyses of E2 target genes suggest that ER regulates many biological pathways and processes in both tissue-type dependent and independent manners. Our results showed that cell lines derived from same tissue display a greater similarity for both profiles of ERBS and gene expression, and that the differential profiles of ER and preferential recruitment of some Co-TFs are the main determinants for the differential regulation of E2 signaling in breast and uterine cancer cells. In order to explore common and distinctive features of ERM-NM-1 (estrogen receptor alpha) binding profiles between breast and uterus, we generated eight ChIP-Seq libraries for the four cell lines (MCF7, T47D, ECC1 and Ishikawa) under two different treatments (E2, ethanol). In addition, we generated four control libraries for the four cell lines. For all treatment libraries, we generated about 7-12 million unique tags each. ER antibody catalog number is (Santa Cruz,sc-543).

Dataset Information

ChIP-Seq of human breast cancer cell lines treated with estrogen and tamoxifen to investigate CTCF binding

Publications

A co-ordinated interaction between CTCF and ER in breast cancer cells.

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