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Homo sapiens

ABSTRACT: Genome-wide mapping of SPDEF and ESR1 binding in MCF-7 cells (ChIP-seq)

PROVIDER: PRJNA212328 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR935442.fastq.gz	Fastqsanger.gz
	SRR935443.fastq.gz	Fastqsanger.gz
	SRR935444.fastq.gz	Fastqsanger.gz
	SRR935445.fastq.gz	Fastqsanger.gz
	SRR935446.fastq.gz	Fastqsanger.gz

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Genome-wide mapping of SPDEF and ESR1 binding in MCF-7 cells (ChIP-seq)

Project description:Using a transcriptional network derived from 2000 breast cancer gene expression profiles we identify the master regulators (MRs) of FGFR2 signalling. To validate the identified regulons, we examined whether there was enrichment of TF binding near the transcription start sites (TSS) of genes found in the regulons of a particular MR. For ESR1 and SPDEF, ChIP-seq experiments were performed in MCF-7 cells, while existing data was analysed for FOXA1 (Hurtado et al. Nature Genetics, 43:27–33, 2010) and GATA3 (Theodorou, et al., Genome Res 23: 12-22, 2013). ChIP-seq experiments were performed on three biological replicates per each transcription factor. For each sample, 36bp single-end reads were obtained. Peak regions were identified in all ChIP-seq TF data sets using the peak caller algorithm MACS (Zhang et al., Genome Biology, 9(9):R137, 2008) with default parameters.

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Genome-wide mapping of NKX2-1 and SPDEF binding sites in A549 lung carcinoma cells by ChIP-seq

Project description:ChIP-seq was performed to identify the binding regions of SPDEF and NKX2-1 in A549 lung carcinoma cells expressing NKX2-1 and SPDEF.

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Modeling the ESR1 tyrosine 537 mutation with CRISPR-Cas9 for mechanistic studies and evaluation of therapeutic approaches for metastatic breast cancer [ChIP-Seq]

Project description:Estrogen receptor-Î± (ERÎ±) is an important driver of breast cancer and is the target for hormonal therapies, anti-estrogens and drugs that limit estrogen biosynthesis (aromatase inhibitors). Mutations in the ESR1 gene identified in metastatic breast cancer provide a potential mechanism for acquired resistance to hormone therapies. We have used CRISPR-Cas9 mediated genome editing in the MCF-7 breast cancer cell line, generating MCF-7-Y537S. MCF-7-Y537S cells encode a wild-type (tyrosine 537) and a mutant (serine 537) allele. Growth of the line is estrogen-independent and expression of ERÎ± target genes is elevated in the absence of estrogen. ER ChIP-seq was carried out to map global ERÎ± binding sites in the presence and absence of estrogen. RNA-seq following estrogen treatment was used for gene expression analysis. We show that expression of ER target genes and ER recruitment to ER binding regions is similar in MCF-7 and MCF-7-Y537S cells, except that ER recruitment to DNA and expression of ER target genes is frequently elevated in the absence of estrogen Hormone depleted MCF-7 LUC /Y537S mutant cells were treated with estrogen (10nM) or ETOH as vehicle control for 45 mins. ErÎ± Chip-seq was performed using Illumnia methodology

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