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Genome-wide Mapping of GATA4 in Breast Cancer MCF-7 Cell Chromatin State.

ABSTRACT: Genome-wide Mapping of GATA4 in Breast Cancer MCF-7 Cell Chromatin State.

PROVIDER: PRJNA1032419 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26533101_1.fastq.gz	Fastqsanger.gz
	SRR26533101_2.fastq.gz	Fastqsanger.gz
	SRR26533102_1.fastq.gz	Fastqsanger.gz
	SRR26533102_2.fastq.gz	Fastqsanger.gz

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Genome-wide Mapping of GATA4 in Breast Cancer MCF-7 Cell Chromatin State.

Project description:To investigate the functional role of GATA4 in breast cancer cells, we employed ChIP-seq analysis to identify GATA4's genome-wide transcription targets. The ChIP experiment began with the use of anti-GATA4 antibodies in MCF-7 cells. Subsequently, GATA4-related DNA was unbiasedly amplified, labeled, and sequenced. Using Illumina Novaseq 6000, we identified numerous GATA4-specific binding peaks. We observed a strong enrichment of GATA4 on the promoters of specific genes involved in classical pathways. This study has provided us with new insights into the role of GATA4 in chromatin state and gene transcription in the context of breast cancer.

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Genome-wide mapping of HIST1H2ac binding sites in MCF-7 cells

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Chromatin state of MCF-7 breast cancer cells treated with proteasome inhibitor MG132 [histone_mod_chip_seq]

Project description:We report whole genome chromatin immunoprecipitation followed by sequencing (ChIP-seq) of histone modifications in MCF-7 breast cancer cells treated with vehicle (UNTR) or the proteasome inhibitor MG132 for 4 (MG4H) or 24 (MG24H) hours. We find that MG132 treatment results in the spreading of the H3-trimethyl lysine 4 mark into gene bodies of a subset of induced genes in MCF-7 cells. The spreading of the H3K4me3 is concomitant with hyperacetylation (H3K27ac, K122ac and K9/14ac) of the corresponding gene TSS. H3 Lysine 36 trimethylation mark is enriched at genes that are induced by MG132. Finally, we show that proteasome inhibition establishes a chromatin state that enhances antiproliferative, while dampening cell proliferative gene expression programs relevant to breast cancer. The study provides a comprehensive resource of histone modifications in proteasome inhibited cells.

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Genome wide mapping in regulatory T cells at steady state

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Genome-Wide Mapping Of Time-Series ChIP-Seq Data For Human ERα Breast Cancer Cell Line (MCF-7)

Project description:We report the genome-wide mapping of time-series ChIP-seq data sets of human breast cancer ERα cell line (MCF-7). The 4 time points cover the 0, 1, 4 and 24 hours, respectively. MCF-7 cells were maintained in a hormone-free medium (phenol red–free MEM with 2 mmol/L L-glutamine, 0.1 mmol/L nonessential amino acids, 50 units/mL penicillin, 50 Ag/mL streptomycin, 6 ng/mL insulin, and 10% charcoal-stripped FBS) for three days. MCF-7 cells were treated with DMSO at the 0 hour time point, and E2 (108 mol/L) at the 1, 4 and 24 hours. 5 x 107 cells were cross-linked with 1% formaldehyde for 10 min, at which point 0.125 M glycine was used to stop the cross-linking. In brief, after crosslinking, cells were treated by lysis buffers and sonicated to fragment the chromatin to a size range of 500-1000 bps. Chromatin fragments were then immunoprecipitated with 10ug of antibody/magnetic beads. The antibodies against ERα were purchased from Santa Cruz Biotechnology (Santa Cruz, sc-8005 X). After immunoprecipitation, washing and elution, ChIP DNA was purified by phenol:chloroform:isoamyl alcohol and solubilized in 70 μl of water. The ChIP DNA sample was run in 12% PAGE and the 100-300 bps DNA fraction was excised and eluted from the gel slice overnight at 4°C in 300 μl of elution buffer (5:1, LoTE buffer (3 mM Tris-HCl, pH 7.5, 0.2 mM EDTA)-7.5 M ammonium acetate) and was purified using a QIAquick purification kit (Qiagen, cat#:28104). The library was constructed using Illumina genomic DNA prep kit by following its protocol (Illumina, cat#:FC-102-1002), clusters were generated on the Illumina cluster station (Illumina, cat#:FC-103-1002), DNA samples (20 nM per sample) quantified by an Agilent Bioanalyzer, were loaded onto Illumina Genome Analyzer IIx (GAIIx) for sequencing according to the manufacturer's protocol. Reads generated from the Illumina GAIIx pipeline were aligned to the Human Genome Assembly (NCBI build 36.1/hg18) using the ELAND algorithm.

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Genome-wide mapping of HIST1H2ac binding sites in MCF-7 cells

Project description:Previously, we have shown that HIST1H2ac is overexpressed in MCF-7 breast cancer cell line. It acts as a master regulator of estrogen receptor alpha-dependent gene expression in ER+ breast cancer cells. In the present study, we investigate the genome-wide protein DNA-binding events of HIST1H2ac protein in MCF-7 breast cancer cell line by over-expressing hemagglutinin (HA)-tagged HIST1H2ac and compared with MCF-7 cells over-expressing HA. The protein-bound DNA was recovered by immunoprecipitation using anti-HA antibody. The ChIP DNA and input DNA were sequenced with an Illumina HiSeq 2000 sequencer.

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Chromatin state of MCF-7 breast cancer cells treated with proteasome inhibitor MG132 [histone_mod_chip_seq]

Project description:Chromatin state of MCF-7 breast cancer cells treated with proteasome inhibitor MG132 [histone_mod_chip_seq]

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Expression data from breast cancer cell lines (MCF-7 and MDA-MB-231)

Project description:We used microarrays to detail the global programme of gene expression for MCF-7 and MDA-MB-231 and revealed the correlation between the methylation state of various genomic components and gene expression level. The expression analyses of the two breast cancer cell lines are a part of the whole study. The summary of our study is as follows: We establish a technique, called modified methylation-specific digital karyotyping (MMSDK) based on methylation-specific digital karyotyping (MSDK) with a novel sequencing approach. Briefly, after a tandem digestion of genomic DNA with a methylation-sensitive mapping enzyme and a fragmenting enzyme, short sequence tags are obtained. These tags are amplified, followed by direct, massively parallel sequencing (Solexa 1G Genome Analyzer). This method allows high-throughput and low-cost genome-wide DNA methylation mapping. We applied this method to investigate global DNA methylation profiles for widely used breast cancer cell lines, MCF-7 and MDA-MB-231, which are representatives for luminal-like and mesenchymal-like cancer types, respectively. By comparison, a highly similar overall DNA methylation pattern was revealed for the two cell lines. However a cohort of individual genomic loci with significantly different DNA methylation profile between two cell lines was identified. Furthermore, we revealed a genome-wide significant correlation between gene expression and the methylation status of gene promoters with CpG islands (CGIs) in the two cancer cell lines, and a correlation of gene expression and the methylation status of promoters without CGIs in MCF-7 cells. Keywords: genetic modification

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