CTCF ChIP-Seq in a panel of 18 cell lines related to ovarian cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE261931 | GEO | 2024/03/26
REPOSITORIES: GEO
Similar Datasets
Project description:CTCF ChIP-Seq in a panel of 18 cell lines related to ovarian cancer
| PRJNA1089603 | ENA
Project description:Assess the baseline expression of the genes in the Oncology Biomarker Panel across the panel of ovarian and cervical cancer cell lines. This data will then be compared to the sensitivity of the cell lines to DDR inhibitors. The expression data will be correlated with the sensitivity of the cell lines to see whether determinants of sensitivity described in the literature translate. A hierarchy of genes will be determined. It is expected that the cells that are more sensitive to DDR inhibitors will have decreased expression of the genes known to be determinants of sensitivity.
2020-05-21 | GSE150942 | GEO
Project description:ChIP-Seq of H4K4me1 in a panel of ovarian cancer related cell lines.
| PRJNA1088145 | ENA
Project description:Analysis of a panel of 41 human ovarian cancer cell lines for the study of ovarian cancer biology, drug response and drug sensitivity.
2012-07-01 | GSE34615 | GEO
Project description:Targeted RNA Sequencing of a panel of ovarian cancer cell lines
| PRJNA634124 | ENA
Project description:CCCTC-binding factor (CTCF) is an 11 zinc fingers transcription factor that functions as both an oncogenic and tumor suppressor, depending on the cancer types, through epigenetic regulation. Epigenetic regulation including DNA methylation and histone modifications are critically involved in cancer metastasis. We then hypothesized that CTCF might play a vital role in epithelial ovarian cancer metastasis. Firstly, we found that CTCF expression was elevated in ovarian cancer tissues compared to non-tumor tissues. The elevated expression of CTCF predicts poor prognosis of ovarian cancer patients. Then, we revealed that CTCF knockdown significantly inhibited the migration, invasion and metastasis of ovarian cancer cells, although it had no effect on cell proliferation and tumor growth, which have been demonstrated with both in vitro and in vivo experiments. More importantly, we observed a higher CTCF expression in metastatic lesions than that in primary lesions from ovarian cancer patients. Mechanically, PCR array demonstrated that CTCF might regulate a series of metastasis associated genes, including CTBP1, SERPINE1 and SRC. Finally, we observed positive correlations between CTCF expression and those three genes in epithelial ovarian cancer specimens. In conclusion, this study demonstrates that CTCF is an oncogene in ovarian cancer to promote tumor metastasis through broadly controlling the expression of metastasis-associated genes. Our findings suggest CTCF could be a novel drug target to treat ovarian cancer by interfering with cancer cell metastasis.
2016-09-01 | GSE85453 | GEO
Project description:H3K27Ac was generated in a panel of 12 ovarian cancer cell lines to identify active regulatory elements in the genome.
2020-08-15 | GSE156275 | GEO
Project description:Epithelial ovarian cancer is a very heterogeneous disease and remains the most lethal gynaecological malignancy in the Western world. Rational therapeutic approaches need to account for interpatient and intratumoral heterogeneity in treatment design. Detailed characterization of in vitro models representing the different histological and molecular subtypes is therefore imperative. Strikingly, from ~100 available ovarian cancer cell lines the origin and which subtype they represent is largely unknown. We have extensively and uniformly characterized 39 ovarian cancer cell lines (with mRNA/microRNA expression, exon sequencing, dose response curves for clinically relevant therapeutics) and obtained all available information on the clinical features and tissue of origin of the original ovarian cancer to refine the putative histological subtypes. From 39 ovarian cell lines, 14 were assigned as high-grade serous, four serous-type, one low-grade serous and 20 non-serous type. Three morphological subtypes (21 Epithelial, 7 Round, 12 Spindle) were identified that showed distinct biological and molecular characteristics, including overexpression of cell movement and migration-associated genes for the Spindle subtype. Clinical validation showed a clear association of the spindle-like tumors with metastasis, advanced stage, suboptimal debulking and poor prognosis. In addition, the morphological subtypes associated with the molecular C1-6 subtypes identified by Tothill et al. [1], Spindle clustered with C1-stromal subtype, Round with C5-mesenchymal and Epithelial with C4 subtype. We provide a uniformly generated data resource for 39 ovarian cancer cell lines, the ovarian cancer cell line panel (OCCP). This should be the basis for selecting models to develop subtype specific treatment approaches, which is very much needed to prolong the survival of ovarian cancer patients. Gene expression was measured for 32 ovarian cancer cell lines using the GeneChip Human Exon 1.0 ST Array (Affymetrix). Morphological subtypes were assigned based on cell morphology, size, growth pattern and proliferation rate during culturing of the cell lines.
2014-09-18 | E-GEOD-53418 | biostudies-arrayexpress
Project description:Epithelial ovarian cancer is a very heterogeneous disease and remains the most lethal gynaecological malignancy in the Western world. Rational therapeutic approaches need to account for interpatient and intratumoral heterogeneity in treatment design. Detailed characterization of in vitro models representing the different histological and molecular subtypes is therefore imperative. Strikingly, from ~100 available ovarian cancer cell lines the origin and which subtype they represent is largely unknown. We have extensively and uniformly characterized 39 ovarian cancer cell lines (with mRNA/microRNA expression, exon sequencing, dose response curves for clinically relevant therapeutics) and obtained all available information on the clinical features and tissue of origin of the original ovarian cancer to refine the putative histological subtypes. From 39 ovarian cell lines, 14 were assigned as high-grade serous, four serous-type, one low-grade serous and 20 non-serous type. Three morphological subtypes (21 Epithelial, 7 Round, 12 Spindle) were identified that showed distinct biological and molecular characteristics, including overexpression of cell movement and migration-associated genes for the Spindle subtype. Clinical validation showed a clear association of the spindle-like tumors with metastasis, advanced stage, suboptimal debulking and poor prognosis. In addition, the morphological subtypes associated with the molecular C1-6 subtypes identified by Tothill et al. [1], Spindle clustered with C1-stromal subtype, Round with C5-mesenchymal and Epithelial with C4 subtype. We provide a uniformly generated data resource for 39 ovarian cancer cell lines, the ovarian cancer cell line panel (OCCP). This should be the basis for selecting models to develop subtype specific treatment approaches, which is very much needed to prolong the survival of ovarian cancer patients.
2014-09-18 | GSE53418 | GEO
Project description:Catalytic activity of the ISWI family of remodelers is critical for nucleosomal organization and transcription factor binding, including the insulator protein CTCF. To define which subcomplex mediates these diverse functions we phenotyped a panel of isogenic mouse stem cell lines each lacking one of six ISWI accessory subunits. Individual deletions of either CERF, RSF1, ACF, WICH or NoRC subcomplexes only moderately affect the chromatin landscape, while removal of the NURF-specific subunit BPTF leads to drastic reduction in chromatin accessibility and Snf2h ATPase localization around CTCF sites. While this reduces distances to the adjacent nucleosomes it only modestly impacts CTCF binding itself. In absence of accessibility, the insulator function of CTCF is nevertheless impaired resulting in lower occupancy of cohesin and cohesin-loading factors, and reduced insulation at these sites, highlighting the need of NURF-mediated remodeling for open chromatin and proper CTCF function. Our comprehensive analysis reveals a specific role for NURF in mediating Snf2h localization and chromatin opening at bound CTCF sites showing that local accessibility is critical for cohesin binding and insulator function.
2024-03-13 | PXD042945 | Pride