Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA342148 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4190180.fastq.gz | Fastqsanger.gz | |||
| SRR4190190.fastq.gz | Fastqsanger.gz | |||
| SRR4190181.fastq.gz | Fastqsanger.gz | |||
| SRR4190191.fastq.gz | Fastqsanger.gz | |||
| SRR4190182.fastq.gz | Fastqsanger.gz |
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Project description:The ets transcription factor ELF5 specifies the differentiation of mammary progenitor cells to establish the milk-secreting lineage. ER- and poor prognosis basal breast cancers arise from this progenitor cell and these cancers express high levels of Elf5. Knockdown of ELF5 expression in basal breast cancer cell lines, or forced expression in luminal breast cancer cell lines, resulted in reduced cell proliferation. Transcript profiling and chromatin immunoprecipitation revealed that the transcriptional activity of ELF5 specified the gene expression patterns that distinguish basal from luminal breast cancer, including suppression of FOXA1, GATA3 and ER, key estrogen-action genes. Tamoxifen treatment of luminal MCF7 cells upregulated Elf5 expression and cells that acquired resistance to Tamoxifen became dependent on ELF5 for proliferation. ELF5 is a regulator of breast cancer cell proliferation, transcriptionally specifies the basal molecular subtype and is utilised by ER+ breast cancer cells to escape proliferative arrest caused by Tamoxifen. ChIP-Seq using an antibody to ELF5, in T47D breast carcinoma cell lines
2012-12-27 | E-GEOD-31216 | biostudies-arrayexpress
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).
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Project description:ChIP-Seq analysis of ER binding sites in MCF7 breast cancer cells
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Project description:We aimed to investigate the chromatin binding activity of DDX3X and DDX54 RNA helicases in human ER -dependent breast cancer MCF7 cells. We run a parallel chromatin binding profiling of ER ChIP-seq. H3K4me3 profiling was used as a quality control of the ChIP-seq procedure.
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Project description:Estrogen Receptor (ER) is a hormonal transcription factor that plays important roles in breast cancer. It functions primarily through binding to the regulatory regions of target genes containing the consensus ERE motifs. In order to identify ER target genes and re-define the ERE motifs we performed ChIP-Seq analysis of ER in MCF7 breast cancer cell line. Applying a novel computational algorithm named Hybrid Motif Sampler (HMS), specifically designed for TFBS motif discovery in ChIP-Seq data, we were able to detect an improved ERE motif and reveal intra-motif dependency especially in neighboring base pairs.
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Project description:Tumor infiltrating lymphocytes (TILs) play a critical role in modulating the immunoediting features in certain malignancies like triple negative breast cancer (TNBC). Nevertheless, much is still unknown concerning the specific responses of tumors when challenged by lymphocyte infiltration. Based on this void, we conducted a immuno-phenotype comparison using mRNA sequencing between the TNBC cell line MDA-MB-231 and the luminal breast cancer cell line MCF7 after both were co-cultured with activated human T-cells. We found that, though the cytokine-induced immune signature of the two cell lines was similar, MDA-MD-231 cells were able to transcribe IDO1 at a significantly higher level than MCF7 cells. Though no differences occurred in upstream JAK/STAT1 signaling or IDO1 mRNA stability between the two cell lines, stimulation with IFNγ was able to differentially induce IDO protein expression and enzymatic activity in ER- cell lines compared to ER+ cell lines. Further experiments show that 5-aza-deoxycytidine treatment was able to reverse suppression of IDO1 expression in MCF7 cells, suggesting DNA methylation as a potential determinant in IDO1 induction. By analyzing TCGA breast cancer datasets, we discovered subtype-specific mRNA and promoter methylation differences in IDO1, with TNBC/basal subtypes exhibiting lower methylation/higher expression and ER+/luminal subtypes exhibiting higher methylation/lower expression. We confirmed this trend of IDO1 methylation by bisulfite pyrosequencing breast cancer cell lines and an independent cohort of primary breast tumors. Taken together, these findings suggest that IDO1 methylation regulates anti-immune responses in breast cancer subtypes and could be used as a predictive biomarker for IDO inhibitor-based immunotherapy. To determine the immunomodulatory effects of cytokines secreted by activated human T-cells on breast cancer cells, we performed RNAseq analysis in MCF7 and MDA-MB-231 cells, after co-culturing them with normal PBMCs activated with anti-CD3/CD28 antibodies in a contact-independent manner. MDA-MB-231 or MCF7 cells were co-cultured with PBMCs alone or the conditioned-media or a combination of both for 24 hrs, and then total RNA was harvest for RNA-seq analysis.
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