Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA284879 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional profiling of drug-tolerant cancer cell subpopulations
| PRJNA273955 | ENA
Project description:Cancer relapse after curative treatment is thought to originate from drug-tolerant and invisible cancer cell subpopulations. Using cancer cell colonies emerging in the presence of drugs (drug-tolerant colonies, DTCs), we found that the drug-tolerant properties of DTCs are lost through a reversible mechanism. To examine whether epigenetic regulation is responsible for the phenotypic changes in DTCs, we performed a genome-wide analysis for relative CpG methylation between the DTCs and untreated colonies derived from MKN45 by NimbleGen Human Meth 385K Prom Plus CpG Arrays. Global changes in the methylation levels were evident in a chromosomal location-dependent manner. The methylation status of the upstream regions of the transcription start sites of the pluripotency-inducing genes showed good agreement with the qRT-PCR data. These results suggest that reversible drug-tolerant properties in DTCs are epigenetically regulated and associated with transcriptional regulation, including pluripotency-inducing factors. Comparison of untreated colonies v.s. DTCs derived from MKN45 cells.
2015-05-26 | E-GEOD-69203 | biostudies-arrayexpress
Project description:Cancer relapse after curative treatment is thought to originate from drug-tolerant and invisible cancer cell subpopulations. Using cancer cell colonies emerging in the presence of drugs (drug-tolerant colonies, DTCs), we found that the drug-tolerant properties of DTCs are lost through a reversible mechanism. To examine whether epigenetic regulation is responsible for the phenotypic changes in DTCs, we performed a genome-wide analysis for relative CpG methylation between the DTCs and untreated colonies derived from MKN45 by NimbleGen Human Meth 385K Prom Plus CpG Arrays. Global changes in the methylation levels were evident in a chromosomal location-dependent manner. The methylation status of the upstream regions of the transcription start sites of the pluripotency-inducing genes showed good agreement with the qRT-PCR data. These results suggest that reversible drug-tolerant properties in DTCs are epigenetically regulated and associated with transcriptional regulation, including pluripotency-inducing factors.
2015-05-26 | GSE69203 | GEO
Project description:Genome-wide DNA methylation analysis of breast cancer
| PRJNA302431 | ENA
Project description:Anti-cancer drug sensitive DNA methylation marker research
| PRJNA137719 | ENA
Project description:Gene methylation profiling of immortalized human mesenchymal stem cells comparing HPV E6/E7-transfected MSCs cells with human telomerase reverse transcriptase (hTERT)- and HPV E6/E7-transfected MSCs. hTERT may increase gene methylation in MSCs. Goal was to determine the effects of different transfected genes on global gene methylation in MSCs.
2011-08-25 | GSE23936 | GEO
Project description:Genome-wide DNA methylation study in bladder cancer
| PRJNA152161 | ENA
Project description:Genome-wide DNA Methylation Analysis Reveals Novel Targets for Drug Development in Mantle Cell Lymphoma
| PRJNA120777 | 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