Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA144915 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Tumor-derived circulating endothelial cell clusters in colorectal cancer
| PRJNA300264 | ENA
Project description:microRNA data in human metastatic versus non-metastatic colorectal cancer tissues
| PRJNA360836 | ENA
Project description:We carried out comprehensive analysis for the miRNA profiling of primary tumor and metastatic lesion which seems to be source of circulating miRNA. We picked up two patients who treated with primary tumor resection initially and received chemotherapy followed by surgical resection of liver metastasis. The total miRNA was isolated from frozen tissue specimens. SurePrint G3 Human miRNA microarray kit Rel.21.0 (Agilent Technologies) contains 2549 human microRNA probes. As previously reported, hsa-miR200c revealed specifically high expression in metastatic sites at both two cases. In two colorectal cancer patients, the frozen primary tumor, normal mucosa and liver-metastatic lesion were analyzed by microRNA microarray.
2015-09-19 | E-GEOD-73178 | biostudies-arrayexpress
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:Exome Sequencing for Metastatic Colorectal Cancer
| PRJNA726023 | ENA
Project description:Genomic landscape of metastatic colorectal cancer
| PRJNA156909 | ENA
Project description:Tumor-educated circulating monocytes are powerful specific biomarkers for diagnosis of colorectal cancer
| PRJNA207669 | ENA
Project description:Whole exome sequencing of circulating tumor cells (CTCs) as a window into metastatic cancer
| PRJNA238372 | ENA
Project description:Whole exome sequencing of circulating tumor cells (CTCs) as a window into metastatic cancer
| PRJNA238373 | ENA