Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA153595 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:RUNX1 and RUNX2 responsiveness in MCF7 breast cancer cells: relationship to estrogen signaling
| PRJNA274487 | ENA
Project description:Cyclin D1 determines estrogen dependent signaling in human breast cancer cell line MCF7
| PRJNA212533 | ENA
Project description:Gene expression profiles of MCF7 breast cancer cells following estrogen and anti-estrogen treatment.
| PRJNA187086 | ENA
Project description:DNA methylation of estrogen regulated enhancers defines endocrine sensitivity in breast cancer
| PRJNA284601 | ENA
Project description:Estrogen signaling and epigenetic modifications, in particular DNA methylation, are involved in regulation of gene expression in breast cancers. Here we investigated a potential regulatory cross-talk between these two pathways by identifying their common target genes and exploring potential underlying molecular mechanisms in human MCF7 breast cancer cells. Principal Findings: Gene expression profiling revealed that the expression of approximately 150 genes was influenced by both 17β-estradiol (E2) and a hypomethylating agent 5-aza-2’-deoxycytidine (DAC). Based on gene ontology (GO), CpG island prediction analysis and previously reported estrogen receptor (ER) binding regions, we selected six genes for further analysis (BTG3, FHL2, PMAIP1, BTG2, CDKN1A and TGFB2). GO analysis suggests that these genes are involved in intracellular signaling cascades, regulation of cell proliferation and apoptosis, while CpG island prediction of promoter regions reveals that the promoters of these genes contain at least one CpG island. Using chromatin immunoprecipitation, we show that ERα is recruited to CpG islands in promoters, but neither in an E2- nor in a DAC-dependent fashion. DAC treatment reactivates the expression of all selected genes although only the promoters of BTG3 and FHL2 genes are methylated, with E2 treatment showing no effect on the methylation status of these promoters. Conclusions: We identified a set of genes regulated by both estrogen signaling and DNA methylation. However, our data does not support a direct molecular interplay of mediators of estrogen and epigenetic signaling at promoters of regulated genes. The aim of the study was to identify genes regulated by estrogen signaling and DNA methylation, using microarray approach. We compared the effects of E2 and DAC on global gene expression profiles in MCF7 cells. By comparing C_E2 (MP5-MP8 average) with C_EtOh samples (MP1-MP4 average), 802 genes were identified as up-regulated by E2, while 851 genes were identified as down-regulated by E2. 1017 genes were identified as up-regulated by DAC, by comparing A_EtOh (MP9-MP12 average) samples with C_EtOh, suggesting that DNA methylation is involved in their regulation. To identify possible common targets, we have compared the DAC up-regulated genes with E2-regulated genes. 88 annotated genes are found to be up-regulated by both E2 and DAC, suggesting that E2 has a hypomethylation-like effect on the regulation of these genes. 58 annotated genes are found to be down-regulated by E2 and up-regulated by DAC, suggesting that E2 has a hypermethylation-like effect on the regulation of these genes.
2012-12-31 | E-GEOD-36683 | biostudies-arrayexpress
Project description:Estrogen signaling and epigenetic modifications, in particular DNA methylation, are involved in regulation of gene expression in breast cancers. Here we investigated a potential regulatory cross-talk between these two pathways by identifying their common target genes and exploring potential underlying molecular mechanisms in human MCF7 breast cancer cells. Principal Findings: Gene expression profiling revealed that the expression of approximately 150 genes was influenced by both 17β-estradiol (E2) and a hypomethylating agent 5-aza-2’-deoxycytidine (DAC). Based on gene ontology (GO), CpG island prediction analysis and previously reported estrogen receptor (ER) binding regions, we selected six genes for further analysis (BTG3, FHL2, PMAIP1, BTG2, CDKN1A and TGFB2). GO analysis suggests that these genes are involved in intracellular signaling cascades, regulation of cell proliferation and apoptosis, while CpG island prediction of promoter regions reveals that the promoters of these genes contain at least one CpG island. Using chromatin immunoprecipitation, we show that ERα is recruited to CpG islands in promoters, but neither in an E2- nor in a DAC-dependent fashion. DAC treatment reactivates the expression of all selected genes although only the promoters of BTG3 and FHL2 genes are methylated, with E2 treatment showing no effect on the methylation status of these promoters. Conclusions: We identified a set of genes regulated by both estrogen signaling and DNA methylation. However, our data does not support a direct molecular interplay of mediators of estrogen and epigenetic signaling at promoters of regulated genes. The aim of the study was to identify genes regulated by estrogen signaling and DNA methylation, using microarray approach.
2012-12-31 | GSE36683 | GEO
Project description:Expression of estrogen receptor (ESR1) determines whether a breast cancer patient receives endocrine therapy as part of their adjuvant care, but does not guarantee patient response. However, the molecular factors that define endocrine response in ESR1-positive breast cancer patients remain poorly understood. Here, we characterize the DNA methylome of endocrine sensitivity and demonstrate the potential impact of differential DNA methylation on endocrine response in breast cancer. We show that DNA hypermethylation occurs predominantly at estrogen-responsive enhancers and is associated with reduced ESR1 binding and decreased gene expression of key regulators of ESR1-activity; thus providing a novel mechanism by which endocrine response is abated in ESR1-positive breast cancers. Conversely, we delineate that ESR1-responsive enhancer hypomethylation is critical in transition from normal mammary epithelial cells to endocrine responsive ESR1-positive cancer. Cumulatively these novel insights highlight the potential of ESR1-responsive enhancer methylation to both predict ESR1-positive disease and stratify ESR1-positive breast cancer patients as responders to endocrine therapy. Methylation profiling with Illumina's HumanMethylation450K array was performed on ESR1-positive hormone sensitive MCF7 cells, and three different well characterised endocrine resistant MCF7-derived cell lines; tamoxifen-resistant (TAMR), fulvestrant-resistant (FASR) and estrogen deprivation resistant (MCF7X) cells. For each cell line two biological replicates were profiled bringing the number of samples to eight.
2015-07-01 | E-GEOD-69118 | biostudies-arrayexpress
Project description:To investigate the function of tyrosyl-DNA phosphodiesterase 2 (TDP2) in estrogen receptor (ER) positive breast cancer, we perfomed bulk and single-cell RNA-seq on MCF7 and MCF7 TDP2-KO cells treated with/without estrogen .
2024-04-17 | GSE225423 | GEO
Project description:The current concept of epigenetic repression is based on one repressor unit corresponding to one silent gene. This notion, however, cannot adequately explain concurrent silencing of multiple loci observed in large chromosome regions. The long-range epigenetic silencing (LRES) can be a frequent occurrence throughout the human genome. To comprehensively characterize the influence of estrogen signaling on LRES, we analyzed transcriptome, methylome, and estrogen receptor alpha (ESR1)-binding datasets from normal breast epithelia and breast cancer cells. This ?omics? approach uncovered 11 large repressive zones (range: 0.35~5.98 megabases), including a 14-gene cluster located on 16p11.2. In normal cells, estrogen signaling induced transient formation of multiple DNA loops in the 16p11.2 region by bringing 14 distant loci to focal ESR1-docking sites for coordinate repression. However, the plasticity of this free DNA movement was reduced in breast cancer cells. Together with the acquisition of DNA methylation and repressive chromatin modifications at the 16p11.2 loci, an inflexible DNA scaffold may be a novel determinant used by breast cancer cells to reinforce estrogen-mediated repression. ChIP-seq: E2-preexposed or DMSO-preexposed mammosphere-derived epithelial cells (MDECs); MCF-7 cells with 4hr of DMSO or E2 stimulation. MeDIP-chip: Methylated DNA from MCF7 cells was immunoprecipitated by the antibody against 5-methyl cytidine. The immunoprecipitated methylated DNA fragments were processed by the NimbleGen Methylation Microarray Service. Methylation analysis was performed on the NimbleGen Two-Array HG18 Promoter Set. mRNA profiling by array: Four sets of total RNA samples from the mammary gland of each 50-day-old rat with prepubertal exposure of BPA. Each sample set includes one BPA-exposed and one sesame oil-exposed rat RNA.
2010-04-29 | E-GEOD-21068 | biostudies-arrayexpress
Project description:Catechol-O-methyl transferase (COMT) is involved in detoxification of catechol estrogens, playing cancer-protective role in cells producing or utilizing estrogen. Moreover, COMT suppressed migration potential of breast cancer cells. To delineate COMT role in metastasis of estrogen receptor dependent BC, we investigated the effect of COMT overexpression on invasion, transcriptome, proteome and interactome of MCF7 cells, a luminal A breast cancer model, stably transduced with lentiviral vector carrying COMT gene (MCF7-COMT). This PRIDE project includes quantitative analysis results for the total proteome LC-DIA-MS/MS experiment evaluating COMT overexpression in MCF7 breast cancer cell line, and results of pulldown analysis of COMT-interacting proteins in MCF7 cells.
2023-01-31 | PXD033833 | Pride