Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA101035 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:human prostate and breast epithelial cell lines under EZH2 adenovirus overexpression
| PRJNA101033 | ENA
Project description:Transcriptional profiling of human prostate and breast epithelial cells comparing control siRNA-treated with EZH2-siRNA treated Keywords: Genetic modification
2007-11-01 | GSE8145 | GEO
Project description:To determine the altered mRNA expression signatures upon overexpressing EZH2 regulated microRNAs in cancer. To identify EZH2 regulated microRNAs in cancer. Two-condition experiment: Each EZH2 microRNA was overexpressed and compared to a control RNA in BT549 breast cancer cells. In DU145 prostate cancer cell EZH2 was knocked down and comapred to EZH2 scrambled siRNA. Other cell lines were monitored for miRNA expression as they are known to have high endogenous levels of EZH2.
2011-10-20 | E-GEOD-26996 | biostudies-arrayexpress
Project description:Genome-wide analysis of human prostate epithelial cell lines
| PRJNA288468 | ENA
Project description:<p>BRCA1 mutations are a hallmark of hereditary ovarian cancer, strongly linked to deficiencies in homologous recombination (HR) DNA repair and impaired DNA replication fork protection. However, its roles in cancer progression beyond maintaining genomic integrity remain poorly understood. Through metabolomics approaches, we found BRCA1-deficiency strikingly increased choline metabolism. Loss of BRCA1 promotes choline uptake through upregulating choline transporter-like protein 4 (CTL4). BRCA1 directly binds and recruits EZH2-mediated H3K27Me3 deposition to CTL4 promoter. CTL4 was therefore overexpressed in ovarian cancer tissues with BRCA1 mutations. Furthermore, BRCA1-deficiency significantly promotes ovarian cancer invasion, while inhibition of CTL4 reverses the high metastatic potential of BRCA1-deficient ovarian cancer cells, suggesting the functionality and specificity of CTL4 as a therapeutic target. Additionally, we discovered that phosphocholine, the choline metabolite increased by CTL4 overexpression, interacted with and stabilized the epithelial-to-mesenchymal transition inducer FAM3C in BRCA1-deficient ovarian cancer cells. Importantly, we identified a potent CTL4 inhibitor, DT-13, which significantly reduces choline metabolism and effectively suppresses metastasis in BRCA1-deficient ovarian cancers. Therefore, our study uncovers a mechanism underlying metastasis in BRCA1-deficient cancers and identifies CTL4 as a therapeutic target for metastatic ovarian cancer patients with BRCA1 mutations.</p>
2026-05-15 | MTBLS12245 | MetaboLights
Project description:Prostate cancer cell lines: non-targeting siRNA versus SChLAP1-siRNA treated
| PRJNA173820 | ENA
Project description:Human Breast Cancer Cell Lines: Control vs. Fn14 or Luciferase siRNA Treated
| PRJNA102239 | ENA
Project description:NDRG1 siRNA and overexpression in breast cell lines
| PRJNA154295 | ENA
Project description:Asthma is a chronic inflammatory airway disease characterized by airway inflammation and remodeling. The role of 15-oxo-5Z,8Z,11Z,13E-eicosatetraenoic acid (15-oxoETE), a 15-HETE metabolite catalyzed by 15-prostaglandin dehydrogenase (15-PGDH), has been relatively unexplored in asthma. In this study, we used RNA-seq to explore the effect of 15-KETE on the transcriptome of airway epithelial cells, aiming to identify its potential downstream targets and mechanisms of action.
2026-05-21 | GSE325003 | GEO
Project description:Transcriptional profiling of human prostate and breast epithelial cells with a time course analysis of EZH2 overexpression of cells at 3, 6, 12, 24, 48, and 72 hrs respectively. Keywords: Genetic modification
2007-11-01 | GSE8144 | GEO