RNA-seq of the human breast cancer ERα-suppressed MCF-7(MCF-7/SP10+) cells and of their internal control MCF-7 (MCF-7/C) cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB19767 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1862940.fastq.gz | Fastqsanger.gz | |||
| ERR1862941.fastq.gz | Fastqsanger.gz | |||
| ERR1862942.fastq.gz | Fastqsanger.gz | |||
| ERR1862937.fastq.gz | Fastqsanger.gz | |||
| ERR1862938.fastq.gz | Fastqsanger.gz |
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Project description:Estrogens receptor a (ERα) is essential for breast tumors,since about seventy percent of breast cancers are detected as ERα positive.Recent studies suggest that ERα is related with the epithelial cell morphology. Recently, it has demonstrated that the suppression of ERα induced epithelial-mesenchymal transition (EMT) in the MCF-7 breast cacner cells. Interestingly, the loss of ERa resulted in strong differences on the gene expression profile of a variety of genes. Therefore, the aim of the RNA-seq is to elucidate the effect of the silencing of ERα on the mRNA levels of a larger variety of genes, thus revealing possible target genes which may be implicated on the aggressive phenotype and behavior of the ERα-suppresed MCF-7/SP10+ breast cancer cells. For this reason total RNA from both MCF-7/SP10+ cells and of their internal control MCF-7/C cells was extracted in 3 biological replicates and 3 technical replicates.
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Project description:We report the genome-wide mapping of time-series ChIP-seq data sets of human ERα cell lines (MCF-7). The 4 time points cover 0, 1, 4 and 24 hours, respectively. MCF7 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. MCF7 cells were treated with DMSO (as 0 hour time point) or E2 (108 mol/L) for 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 crosslinking. In brief, after crosslinking, cells were treated by lysis buffers and sonicated to fragment the chromatin to a size range of 500bp-1kb. 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 100-300bp 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 ELAND algorithm. Experiments on human ERα breat cancer cell lines (MCF-7) in 4 time points.
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Project description:RNA-seq: Gene expression profiling in MCF-7 cells treated with vehicle (0), estradiol (E2), the Selective ER Modulator 4-hydroxytamoxifen (OHT), or the pure antiestrogen fulvestrant (ICI). ChIP-seq: Genome-wide DNA binding profile of ERα and SUMO2/3 in MCF-7 cells treated with vehicle, E2 or ICI.
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Project description:To identify microRNAs impacting estrogen receptor ERα expression in breast cancer, we have screened ER-positive breast cancer cells with a library of pre-miRs, and systematically monitored the ERα expression by protein lysate microarrays. There was a significant enrichment of the in silico predicted ERα targeting microRNAs among the hits. The most potent pre-miRs miR-18a/b, miR-193b, miR-206, and miR-302c, were confirmed to directly target ERα and to repress estrogen-responsive genes. The effect of miRNA overexpression on gene expression profile of MCF-7 cells was studied. Furthermore, miR-18a and miR-18b showed increased expression in ERα-negative as compared to ERα-positive clinical tumors. In summary, we present systematic and direct functional and correlative clinical evidence on microRNAs inhibiting ERα signaling in breast cancer.
2009-08-18 | GSE14847 | GEO
Project description:Estrogen Receptor alpha (ERα), a nuclear receptor with transcriptional activity, is a master regulator of estrogen signaling, widely known as therapeutic target in hormone-responsive breast cancer (BC). Moreover, ERα is highly expressed in approximately 80% of High Grade Serous Ovarian Cancer (HGSOC), the most common epithelial ovarian carcinoma. Despite some promising clinical trials evaluating endocrine therapy in this type of tumor, the role of ERα is still unknown. Epigenetic changes, such as DNA methylation, are emerging as key contributing factors to carcinogenesis. Disruptor of telomeric silencing-1-like (DOT1L), the only known histone methyl transferase capable to produce H3K79 mono, di and tri-methylation, modulates ERα actions in hormone-responsive BC. Considering this evidence, ERα-DOT1L association was confirmed in ERα-positive OC cells, PEO1 and PEO4, by Co-IP. DOT1L pharmacological inhibition by EPZ004777 (EPZ) revealed the involvement of this epigenetic enzyme in cell proliferation, cell cycle progression and apoptosis. Transcriptome profiling after ICI (a Selective Estrogen Receptor Degrader) and EPZ treatment, in both cell lines, has underlined a deep impact of both compounds on ERα-modulated genes, including the down-regulation of ERα itself. On the other hand, functional analysis showed that commonly affected transcripts are involved in different cellular processes, such as cancer cell survival, chemoresistance and cell cycle progression. Moreover, ChIP-qPCR performed on ERα promoter highlighted ERα and DOT1L co-localization, both in PEO1 and in PEO4 cells, which was reduced after EPZ treatment, suggesting a role of this complex on receptor transcriptional activity. In addition, drug combination studies performed with EPZ and ICI showed an additive effect in cell growth inhibition. Taken together, these results suggest DOT1L as a potential therapeutic target in the treatment of OC.
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Project description:We show that most binding events of NR2F2 occur together with the ERα binding sites.To address the functional relationship between NR2F2 and ERα, we assessed the role of NR2F2 in oestrogen-induced growth in ER positive cell line MCF-7. The MTT experiment showed that inhibition of NR2F2 prevented the oestrogen-induced proliferation of MCF-7 cells.To further explore the effect of NR2F2 on estrogen response, We expanded our knockdown studies by performing RNA-seq analysis for MCF-7 cells transfected with control or NR2F2 shRNAs with or without E2.
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Project description:The molecular mechanisms of endocrine resistance in breast cancer remain poorly understood. Here we used PRO-seq to map the location of hundreds of genes and thousands of distal enhancers whose activities differ between endocrine sensitive and resistant MCF-7 cells. Our genome-wide screen identified a 16-fold transcriptional increase in glial-cell line derived neurotrophic factor (GDNF), a RET tyrosine kinase receptor ligand, which is both necessary and sufficient for resistance in MCF-7 cells. GDNF causes endocrine resistance by switching the active state of a bi-stable feedback loop from ERα signaling to GDNF-RET signaling. To catalyze this switch, we found that GDNF directly downregulates ERα transcription and activates the transcription factor EGR1, which, in turn, induces GDNF expression. Remarkably, both MCF-7 cells and ER+ primary tumors appear poised for endocrine resistance via the RET signaling pathway, but lack robust RET ligand expression and only develop resistance upon expression of GDNF or other RET ligands.
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