Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA152943 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression data from EZH2 inhibitor treated Non-Hodgkins Lymphoma cell lines
| PRJNA213485 | 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:Gene expression profiling of EZH2 mutant and wild type DLBCL cell lines treated with EZH2 inhibitor
| PRJNA175452 | ENA
Project description:Expresssion data from reovirus treated breast cancer cell lines
| PRJNA286858 | ENA
Project description:Breast cancer cell lines treated with eribulin and paclitaxel
| PRJNA219068 | ENA
Project description:Expression data in NK150460 treated breast cancer cell lines
| PRJNA261441 | ENA
Project description:Loss of H3K27me3 repressive chromatin histone marks, maintained by the histone methyltransferase (HKMT) EZH2, may lead to reversal of epigenetic silencing in tumor cells and have therapeutic potential. Using a cell-based assay, we have identified three compounds from a HKMT inhibitor chemical library which re-express H3K27me3 mediated, silenced genes. Chromatin immunoprecipitation verified a decrease in silencing marks (H3K27me3, H3K9me3) and importantly an increase in active marks (H3K4me2/3, H3K27ac) at the promoter of re-expressed genes. Compound treated breast tumor cells induced enrichment for genome-wide changes in expression of known target genes for EZH2 and induced cell growth inhibition: with most sensitive breast tumor cell lines having low EZH2 protein expression, while a normal epithelial breast line was least sensitive.
2013-08-27 | GSE36131 | GEO
Project description:Loss of H3K27me3 repressive chromatin histone marks, maintained by the histone methyltransferase (HKMT) EZH2, may lead to reversal of epigenetic silencing in tumor cells and have therapeutic potential. Using a cell-based assay, we have identified three compounds from a HKMT inhibitor chemical library which re-express H3K27me3 mediated, silenced genes. Chromatin immunoprecipitation verified a decrease in silencing marks (H3K27me3, H3K9me3) and importantly an increase in active marks (H3K4me2/3, H3K27ac) at the promoter of re-expressed genes. Compound treated breast tumor cells induced enrichment for genome-wide changes in expression of known target genes for EZH2 and induced cell growth inhibition: with most sensitive breast tumor cell lines having low EZH2 protein expression, while a normal epithelial breast line was least sensitive. Agilent SurePrint G3 Human 8x60k two-colour microarrays were used to profile gene expression changes induced by treatment with drug compounds in MDA MB-231 cells, both at 24h and 48h. 4 replicates were used for each drug, time combination. A separate untreated control sample was used for comparison with each replicate.
2013-08-27 | E-GEOD-36131 | biostudies-arrayexpress