Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA105685 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Metaphase comparative genomic hybridisation (CGH) studies indicate that chromosomes 4, 5, 6, 13, 14, 15 and 18 are frequently deleted in primary ovarian cancers (OC). Therefore, we used microcell-mediated chromosome transfer (MMCT) to establish the functional effects of transferring normal copies of these chromosomes into two epithelial OC cell lines. The in vitro neoplastic phenotype (measured as anchorage dependent and independent growth and invasion) was compared between recipient OC cell lines and multiple MMCT hybrids. Chromosomes 6 and 18 showed strong evidence of functional, neoplastic suppression for multiple hybrids in both cell lines. We also found evidence in one cancer cell line suggesting that chromosomes 4, 13 and 14 may also cause functional suppression. Array CGH and microsatellite analyses were used to characterise the extent of genomic transfer in chromosome 6 and 18 hybrids. A 35Mb deletion on chromosome 6 in two hybrids from one cell line mapped the candidate region proximal to 6q15 and distal to 6q22.2; and an approximate 10Mb candidate region spanning the centromere on chromosome 18 was identified in another two hybrids from the other cell line. These data confirm reported functional effects of chromosome 6 in OC cell lines; but to our knowledge, this is the first time that functional suppression for chromosome18 has been reported. This suggests that these chromosomes may harbour genes that behave as tumour suppressors. The future identification of these genes may have a significant impact on the understanding and treatment of the disease and the identification of novel therapeutic targets. Four clones from chr 6 and chr 18 hybrids that were transferred by MMCT successfully were mapped by CGH microarray to identified transferred regions that induced neoplastic suppression in epithelial ovarian cancer cell lines (TOV21G and TOV112D).
2008-08-19 | E-GEOD-11872 | 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:Metaphase comparative genomic hybridisation (CGH) studies indicate that chromosomes 4, 5, 6, 13, 14, 15 and 18 are frequently deleted in primary ovarian cancers (OC). Therefore, we used microcell-mediated chromosome transfer (MMCT) to establish the functional effects of transferring normal copies of these chromosomes into two epithelial OC cell lines. The in vitro neoplastic phenotype (measured as anchorage dependent and independent growth and invasion) was compared between recipient OC cell lines and multiple MMCT hybrids. Chromosomes 6 and 18 showed strong evidence of functional, neoplastic suppression for multiple hybrids in both cell lines. We also found evidence in one cancer cell line suggesting that chromosomes 4, 13 and 14 may also cause functional suppression. Array CGH and microsatellite analyses were used to characterise the extent of genomic transfer in chromosome 6 and 18 hybrids. A 35Mb deletion on chromosome 6 in two hybrids from one cell line mapped the candidate region proximal to 6q15 and distal to 6q22.2; and an approximate 10Mb candidate region spanning the centromere on chromosome 18 was identified in another two hybrids from the other cell line. These data confirm reported functional effects of chromosome 6 in OC cell lines; but to our knowledge, this is the first time that functional suppression for chromosome18 has been reported. This suggests that these chromosomes may harbour genes that behave as tumour suppressors. The future identification of these genes may have a significant impact on the understanding and treatment of the disease and the identification of novel therapeutic targets.
2008-08-19 | GSE11872 | GEO
Project description:The generation of pancreatic organoids from human pluripotent stem cells represents a major breakthrough for regenerative medicine and the modeling of diseases such as diabetes. However, current approaches remain inefficient due to lengthy multi-step differentiation protocols and limited functional maturity in the organoids. In this study, we overcome these challenges using multi-phase optimization screens to achieve rapid generation of functionally mature pancreatic organoids from a stable endocrine progenitor culture. We conducted stepwise culture condition screens that enabled the stable culture of multiple pancreatic progenitor cell states, including the unprecedented stable propagation of NEUROD1-expressing endocrine progenitor-like cells (EpSCs). Further transcriptomic profiling of EpSC confirmed similarity of that to previously reported endocrine progenitor populations. Using EpSCs, we significantly reduced the number of steps and timing required to generate pancreatic organoids, enabling rapid testing of conditions for organoid maturation. Utilizing this optimized protocol, we further tested conditions to promote pancreatic organoid maturation. We identified that exosome-delivered WNT5B, in combination with RSPO1 (exoW/R), could strongly induce non-canonical WNT/JNK signaling, promoting pancreatic organoid maturation. This combinatorial exosome treatment enhances epithelial organization, reduces immature cell states, and significantly improves glucose responsiveness and insulin secretion. Collectively, our work establishes a robust pancreatic differentiation platform that integrates long-term progenitor expansion with optimized organoid maturation. This system provides a reproducible experimental framework for studying pancreatic development, investigating disease mechanisms, and facilitating future translational applications involving pancreatic organoids.
2026-09-24 | GSE348014 | GEO
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:Ovarian cancer is one of the most deadly cancers accounting for only 3% of diagnosed cancers, but is the fifth leading cause of cancer deaths among woman; however, the progression of ovarian cancer is poorly understood. To study and further understand the early events that lead to epithelial derived ovarian cancer, we previously developed a cell model of progressive ovarian cancer. Mouse ovarian surface epithelial (MOSE) cells have undergone spontaneous transformation in cell culture and represent pre-neoplastic, non-tumorigenic to an aggressive malignant phenotype. Microarray analysis was performed with RNA isolated from different stages of MOSE cells to examine changes in gene expression as MOSE cells transition from a pre-neoplastic to a malignant state. RNA was isolated from MOSE early cell representing a pre-neoplastic, non-malignant stage, MOSE Intermediate cells representing a noeplastic, pre-invasive state, and MOSE Late cells representing a malignant, invasive stage. Three biological replicates were used to take into account variations within the heterogeneous cultures.
2011-03-03 | E-GEOD-24789 | biostudies-arrayexpress
Project description:Expression profiling identifies genes involved in neoplastic transformation of serous ovarian cancer
| PRJNA118973 | ENA
Project description:The human kinome is incolved in multiple function in the life cycle of cells, and ther differntial expression in cacner suggests that protein kinases play an important role in tumor progression and proliferation. To delineate pathways that may be important for neoplastic change in women at high risk for ovarian cancer, we compared the expression signature of surface kinases in normal ovarian surface epithelium with ovarian epithelium from patients at high risk, and epithelial ovarian cancer using Affymetrix expresion array HG U133Plus2. A total of 18 ovarian samples were collected. The number of samples and subjects for each group were: 5 cancer samples (5 subjects), 6 normal samples (4 patients) and 7 high-risk samples (5 subjects). After the initial inspection, one cancer sample (Sample 9) was excluded from the statistical analysis due to a poor RNA quality.
2009-04-07 | E-GEOD-15578 | biostudies-arrayexpress
Project description: Not available
| S-EPMC2531291 | biostudies-literature
Project description:Ovarian cancer is one of the most deadly cancers accounting for only 3% of diagnosed cancers, but is the fifth leading cause of cancer deaths among woman; however, the progression of ovarian cancer is poorly understood. To study and further understand the early events that lead to epithelial derived ovarian cancer, we previously developed a cell model of progressive ovarian cancer. Mouse ovarian surface epithelial (MOSE) cells have undergone spontaneous transformation in cell culture and represent pre-neoplastic, non-tumorigenic to an aggressive malignant phenotype. Microarray analysis was performed with RNA isolated from different stages of MOSE cells to examine changes in gene expression as MOSE cells transition from a pre-neoplastic to a malignant state.
2011-03-03 | GSE24789 | GEO