Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA427659 | ENA |
REPOSITORIES: ENA
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Project description:Human PBMCs Transcriptome co-culture with Head and Neck cancer cells line.
| PRJNA427658 | ENA
Project description:Homo sapiens Transcriptome co-culture with Lung cancer cell lines.
| PRJNA427748 | ENA
Project description:(Objectives) The goal of this study is to investigate paracrine effect of peripheral blood mononuclear cells (PBMCs) on ovarian cancer cell lines. (Methods) Transcription profiles of PBMC (control) and PBMC co-cultured with ovarian cancer cell lines (treatment) were generated by deep sequencing, in triplicate, using Illumina HiSeq X Ten. (Results and Conclusions) Transcriptome analysis of PBMCs has revealed the expression change when co-cultured with EOC cell lines with significantly in up-regulated genes; CDKN1B, GIMAP8 and SNN. The qRT-PCR validation have indicated that GIMAP8 was high expressed in EOC patients when compared with healthy female. We summarized that PBMCs were changed their expression as a result of paracrine signals from ovarian cancer cells.
2020-12-31 | GSE110745 | GEO
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:Effect of co-culture with macrophages on two colon cancer cell lines.
| PRJNA241038 | ENA
Project description:Expression profiling of ovarian cancer cell lines
| PRJNA177228 | ENA
Project description:Ovarian Cancer Cell Lines pre-microRNA Transfection
| PRJNA113075 | ENA