ChIP-seq of MDA-MB-134 cell line
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE51022 | GEO | 2014/01/15
SECONDARY ACCESSION(S): PRJNA219645
REPOSITORIES: GEO
Similar Datasets
Project description:We performed ChIP seq experiment in MDA-MB-134 cell line in order to map the estrogen receptor alpha (ER) binding sites following the estrogen treatment in an ILC model. We have characterized the genome wide recruit of ER and scaned the binding sites for the presence of cofactor motifs. The binding peaks were also correlated to E2 regulated genes in this ILC model. Four samples were subjected to high throughput sequencing: E-ER (estrogen treated followed by ER IP), E-IgG (estrogen treated followed by IgG), V-ER (EtOH treated followed by ER IP) and Input (MCF7 genomic DNA)
2014-01-15 | E-GEOD-51022 | biostudies-arrayexpress
Project description:This experiment aims to study transcriptional alterations induced by reconstitution of wild type E-cadherin expression in human lobular breast cancer cells harbouring deleterious, somatic CDH-1 mutations Two cell lines (IPH-926 and MDA-MB-134) expressing synthetic Ecad (EcadEGFP) or not (EGFP) were compared against each other. Analysis were conducted in triplicates (IPH-926) and quadruplicates (MDA-MB-134), respectively.
2014-03-04 | E-GEOD-55529 | biostudies-arrayexpress
Project description:We have utilized ChIPseq to identify the ER-beta cistrome in ER-beta expressing MDA-MB-231 triple negative breast cancer cells. ER-beta has been identified as a tumor suppressor in breast cancer and recent reports have demonstrated that ER-beta protein is detectable at moderate to high levels in approximately 30% of triple negative breast tumors. Increased expression of ER-beta in triple negative breast cancer has also been reported to be associated with improved recurrence-free survival. Treatment of ER-beta expressing triple negative breast cancer cells with estrogen, or the ER-beta selective agonist, LY500307, results in decreased cell proliferation, invasion and migration. To begin to identify the molecular mechanisms by which ER-beta elicits tumor suppressive effects in triple negative breast cancer, we performed ChIPseq studies and identified the genome-wide binding sites for ER-beta following exposure to 1nM estrogen or 10nM LY500307 for 3 hours. Over 28,000 and 10,000 unique ER-beta binding sites were identifed in response to these two ligands respectively. The top transcription factor motifs identified under both treatment conditions were estrogen response elements and AP1 response elements. The majority of ER-beta binding sites were found at enhancer regions located within introns or intergenic chromatin regions followed by gene promoters.
2018-08-23 | GSE108979 | GEO
Project description:Androgen receptor (AR) is expressed in 60-70% of breast cancers independent of estrogen receptor (ER) expression, however its function in breast cancer is largely unknown. Our study identified the high level of AR in ERâ/HER2+ breast tumors and andorgen and AR greatly stimulated growth of MDA-MB-453 breast cancer cells. To define the genome-wide AR binding sites, we performed AR ChIP-seq using MDA-MB-453 breast cancer cells followig stimulation of DHT. We also identified FOXA1 is a crucial AR cofactor in MDA-MB-453 cells and the FOXA cistrome showed signaficant overlap with AR at both early and late time points of DHT stimulation.
2011-07-11 | GSE28788 | GEO
Project description:Background: Invasive lobular breast carcinoma (ILC) is a histological subtype of breast cancer that is characterized by loss of E-cadherin, and high expression of estrogen receptor alpha (ER). Many patients with ILC are effectively treated with adjuvant aromatase inhibitors (AIs), however, acquired AI resistance remains a significant problem. Methods: To identify underlying mechanisms of acquired antiestrogen resistance in ILC, we developed a total of 6 long-term estrogen-deprived (LTED) variant cell lines of the human ILC cell lines SUM44PE (SUM44; 2 lines) and MDA-MB-134VI (MM134; 4 lines). To better understand mechanisms of AI resistance in these models, we performed transcriptional profiling analysis by RNA-sequencing. Results: MM134 LTED cells expressed ER at decreased level and lost growth response to estradiol, while SUM44 LTED cells retained partial ER activity. Our transcriptional profiling analysis identified shared activation of lipid metabolism across all 6 independent models. However, the underlying basis of this signature was distinct between models. Oxysterols were able to promote the proliferation of SUM44 LTED cells, but not MM134 LTED. In contrast, MM134 LTED cells displayed high expression of the Sterol regulatory element-binding protein 1 (SREBP1), a regulator of fatty acid and cholesterol synthesis, and were hypersensitive to genetic or pharmacological inhibition of SREBPs. Several SREBP1 downstream targets involved in fatty acid synthesis, including FASN, were induced, and MM134 LTED cells were more sensitive to etomoxir, an inhibitor of the rate-limiting enzyme in β-oxidation, than their respective parental control cells. Conclusions: Our characterization of a unique series of AI-resistant ILC models identifies a lipogenic phenotype, including overexpression of SREBP1. This novel metabolic target deserves further study for the prevention and treatment of AI-resistance for patients with ILC.
2018-08-30 | GSE116744 | GEO
Project description:Androgen receptor (AR) is expressed in 60-70% of breast cancers independent of estrogen receptor (ER) expression, however its function in breast cancer is largely unknown. Our study identified the high level of AR in ERâ??/HER2+ breast tumors and andorgen and AR greatly stimulated growth of MDA-MB-453 breast cancer cells. To define the genome-wide AR binding sites, we performed AR ChIP-seq using MDA-MB-453 breast cancer cells followig stimulation of DHT. We also identified FOXA1 is a crucial AR cofactor in MDA-MB-453 cells and the FOXA cistrome showed signaficant overlap with AR at both early and late time points of DHT stimulation. AR ChIP was performed in MDA-MB-453 breast cancer cells following 5a-dihydrotestosterone (DHT) stimulation for 4h and 16h respectively. FOXA1 ChIP-seq was performed after 4h DHT stimulation in MDA-MB-453 cells.
2011-07-11 | E-GEOD-28788 | biostudies-arrayexpress
Project description: Not available
| S-ECPF-GEOD-55529 | biostudies-other
Project description:Invasive lobular carcinoma (ILC) is the most frequent specific histological subtype of breast cancer (BC). It has distinct clinical features from other estrogen receptor positive (ER+) BCs but the molecular mechanisms underlying the characteristic biology are unclear because we lack experimental models to study it. Here, we generate xenograft models with ILC-derived SUM-44 PE and MDA-MB-134-VI cells by grafting them to mouse milk ducts that recapitulate the human disease including metastasis to visceral organs. Transcriptomic analysis of intraductal ER+ PDXs reveals extracellular matrix modulation as an ILC-specific trait. This signature confirms in patient datasets. The collagen modifying enzyme LOXL1 is overexpressed specifically in ILCs by tumor cells; treatment with a LOX inhibitor, BAPN, and LOXL1 silencing decrease tumor growth and inhibit metastasis by disrupting ECM structure/fibrils with down modulation of ER, IGFR, and FGFR signaling. Hence inhibition of LOXL1 is a promising therapeutic strategy for ILC.
2020-12-09 | GSE149675 | GEO
Project description:Invasive lobular carcinoma (ILC) is the most frequent specific histological subtype of breast cancer (BC). It has distinct clinical features from other estrogen receptor positive (ER+) BCs but the molecular mechanisms underlying the characteristic biology are unclear because we lack experimental models to study it. Here, we generate xenograft models with ILC-derived SUM-44 PE and MDA-MB-134-VI cells by grafting them to mouse milk ducts that recapitulate the human disease including metastasis to visceral organs. Transcriptomic analysis of intraductal ER+ PDXs reveals extracellular matrix modulation as an ILC-specific trait. This signature confirms in patient datasets. The collagen modifying enzyme LOXL1 is overexpressed specifically in ILCs by tumor cells; treatment with a LOX inhibitor, BAPN, and LOXL1 silencing decrease tumor growth and inhibit metastasis by disrupting ECM structure/fibrils with down modulation of ER, IGFR, and FGFR signaling. Hence inhibition of LOXL1 is a promising therapeutic strategy for ILC.
2020-12-09 | GSE149671 | GEO
Project description:Super-enhancers are defined by peaks in H3K27 acetylation and H3K4 mono-methylation, and the lack of H3K4 tri-methylation. They have been found to play a role in oncogene transcription and tumour maintenance. Using ChIP-Seq, we profiled H3K27ac, H3K4me and H3K4me3 binding in CHP-134 neuroblastoma cells. We identified H3K27ac, H3K4me and H3K4me3 binding sites in the CHP-134 neuroblastoma cell line.
2019-06-23 | GSE113139 | GEO