Ovarian cancer cell lines [Baseline profiling]
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE34615 | GEO | 2012/07/01
SECONDARY ACCESSION(S): PRJNA150449
REPOSITORIES: GEO
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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. Ovarian cancer cell lines were either obtained from the American Type Culture Collection (ATCC, Manassas, VA) (CAOV3, OV90, OVCAR3, SKOV3, TOV112D), the European Collection of Cell Cultures, Salisbury, England (A2780CP, A2780S); Kyoto University, Kyoto, Japan (CHI, CHIcisR, M41, M41CSR, Tyknu, and TyknuCisR), or were kind gifts from Dr. Patricia Kruk, Department of Pathology, College of Medicine, University of South Florida, Tampa, FL; and Susan Murphy, PhD, Dept of OBGYN/Division of GYN Oncology, Duke University, Durham, NC (A2008, C13, CAOV2, FUOV1, HeyA8, IGR-OV1, IMCC3, IMCC5, MCAS, OV2008, OVCA420, OVCA429, OVCA432, OVCA433, OVCAR4, OVCAR5, OVCAR8, Dov13, BG1, Ovary1847, OVCAR10, OVCAR2, SK-OV-4). Cell lines were maintained in RPMI-1640 (Invitrogen; Carlsbad, California) supplemented with 10% fetal bovine serum (Fisher Scientific; Pittsburg, PN), 1% sodium pyruvate, 1% penicillin/streptomycin (Cellgro; Manassas, VA), and 1% nonessential amino acids (HyClone; Hudson, New Hampshire). Mycoplasma testing was performed every six months following manufacturer’s protocol (Lonza, Rockland ME).
2012-06-30 | E-GEOD-34615 | biostudies-arrayexpress
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:PD-0332991 is a selective inhibitor of the CDK4/6 kinases with the ability to block retinoblastoma (Rb) phosphorylation in the low nanomolar range. Here we investigate the role of CDK4/6 inhibition in human ovarian cancer. We examined the effects of PD-0332991 on proliferation, cell-cycle, apoptosis, and Rb phosphorylation using a panel of 40 established human ovarian cancer cell lines. Molecular markers for response prediction, including p16 and Rb, were studied using gene expression profiling, Western blot, and arrayCGH. Multiple drug effect analysis was used to study interactions with chemotherapeutic drugs. Expression of p16 and Rb was studied using immunohistochemistry in a large clinical cohort ovarian cancer patients. Concentration-dependent anti-proliferative effects of PD-0332991were seen in all ovarian cancer cell lines, but varied significantly between individual lines. Rb proficient cell lines with low p16 expression were most responsive to CDK4/6 inhibition. Copy number variations of CDKN2A, Rb, CCNE1, and CCND1 were associated with response to PD-0332991. CDK4/6 inhibition induced G0/G1 cell cycle arrest, blocked Rb phosphorylation in a concentration and time dependent manner, and enhanced the effects of chemotherapy. Rb proficiency with low p16 expression was seen in 97/262 (37%) of ovarian cancer patients and associated with adverse clinical outcome (progression free survival, adjusted relative risk 1.49, 95%CI 0.99-2.22, p =0.054). PD-0332991 shows promising biologic activity in ovarian cancer cell lines. Assessment of Rb and p16 expression may help select patients most likely to benefit from CDK4/6 inhibition in ovarian cancer. Gene expression of 40 individual ovarian cell lines relative to an ovarian cell line reference mix containing equal amounts of 41 ovarian cell lines (including OCC-1 which was later identified as originating from mouse). The expression data was correllated with cell line growth response to CDK 4/6 inhibitor PD-0332991 to identify genes associated with drug sensitivity and resistance.
2011-01-22 | E-GEOD-26805 | biostudies-arrayexpress
Project description:The inability to establish stable cell lines from the vast majority of human tumors has limited the use of in vitro models to study human cancer. Currently available tumor cell lines fail to represent the biological diversity of human tumors. We have developed a cell culture medium that enabled us to routinely establish cell lines from diverse subtypes of ovarian tumors. Importantly, the twenty-five ovarian tumor cell lines described here retain the genomic landscape, histopathology, and molecular features of the original tumors. Furthermore, the molecular profile and drug response of these cell lines correlated with distinct groups of primary tumors with different outcomes. Thus, tumor cell lines derived using this methodology represent a significantly improved new platform to study human tumor biology and treatment. 41 samples were analyzed in singlicate. DNA was extracted from 16 OCI cell lines and the 16 uncultured tumor tissue samples from which they were derived. DNA was also extracted from 9 standard ovarian cancer cell lines.
2015-06-16 | E-GEOD-40787 | biostudies-arrayexpress
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:We sought to detect predictive markers related to a Src kinase inhibitor (saracatinib) sensitivity in ovarian cancer. Cell proliferation assays assigned 18 ovarian cancer cell lines to sensitive or resistant to this drug. Using baseline gene expression data from these 18 cell lines, we sought to identify differentially expressed genes correlated with saracatinib sensitivity. We also used SNP array data from 7 cell lines to detect differentically affected genomic locations.
2017-03-05 | GSE55628 | GEO
Project description:Drug resistance poses a major challenge to ovarian cancer treatment. Understanding mechanisms of drug resistance is important for finding new therapeutic targets. In the present work, a cisplatin-resistant ovarian cancer cell line A2780-DR was established with a resistance index of 6.64. The cellular accumulation of cisplatin was significantly reduced in A2780-DR cells as compared to A2780 cells consistent with the general character of drug resistance. Quantitative proteomic analysis identified 340 differentially expressed proteins between A2780 and A2780-DR cells, which involve in diverse cellular processes, including metabolic process, cellular component biogenesis, cellular processes and stress responses. Expression levels of Ras-related proteins Rab 5C and Rab 11B in A2780-DR cells were lower than those in A2780 cells as confirmed by real-time quantitative PCR and western blotting. The short hairpin (sh)RNA-mediated knockdown of Rab 5C in A2780 cells resulted in markedly increased resistance to cisplatin whereas overexpression of Rab 5C in A2780-DR cells increases sensitivity to cisplatin, demonstrating that Rab 5C-dependent endocytosis plays an important role in cisplatin resistance. Our results also showed that expressions of glycolytic enzymes PKM, GPI, Aldolase, LDH, and PGK were down-regulated in drug resistant cells, indicating drug resistance in ovarian cancer is directly associated with a decrease in glycolysis. Furthermore, it was found that glutathione reductase were up-regulated in A2780-DR, while vimentin, HSP90, and Annexin A1 and A2 were down-regulated. Taken together, our results suggest that drug resistance in ovarian cancer cell line A2780 is caused by multifactorial traits, including the down-regulation of Rab 5C-dependent endocytosis of cisplatin, glycolytic enzymes and vimentin, and up-regulation of antioxidant proteins, suggesting Rab 5C is a potential target for treatment of drug-resistant ovarian cancer. This constitutes a further step towards a comprehensive understanding of drug resistance in ovarian cancer.
2016-07-06 | PXD001176 | Pride
Project description:Transcriptome profiling of matched ovarian cancer cell lines with in vivo platinum sensitivity and resistance by next-generation sequencing
2011-07-31 | E-MTAB-691 | biostudies-arrayexpress
Project description:Drug resistance poses a major challenge to ovarian cancer treatment. Understanding mechanisms of drug resistance is important for finding new therapeutic targets. In the present work, a cisplatin-resistant ovarian cancer cell line A2780-DR was established with a resistance index of 6.64. The cellular accumulation of cisplatin was significantly reduced in A2780-DR cells as compared to A2780 cells consistent with the general character of drug resistance. Quantitative proteomic analysis identified 340 differentially expressed proteins between A2780 and A2780-DR cells, which involve in diverse cellular processes, including metabolic process, cellular component biogenesis, cellular processes and stress responses. Expression levels of Ras-related proteins Rab 5C and Rab 11B in A2780-DR cells were lower than those in A2780 cells as confirmed by real-time quantitative PCR and western blotting. The short hairpin (sh)RNA-mediated knockdown of Rab 5C in A2780 cells resulted in markedly increased resistance to cisplatin whereas overexpression of Rab 5C in A2780-DR cells increases sensitivity to cisplatin, demonstrating that Rab 5C-dependent endocytosis plays an important role in cisplatin resistance. Our results also showed that expressions of glycolytic enzymes PKM, GPI, Aldolase, LDH, and PGK were down-regulated in drug resistant cells, indicating drug resistance in ovarian cancer is directly associated with a decrease in glycolysis. Furthermore, it was found that glutathione reductase were up-regulated in A2780-DR, while vimentin, HSP90, and Annexin A1 and A2 were down-regulated. Taken together, our results suggest that drug resistance in ovarian cancer cell line A2780 is caused by multifactorial traits, including the down-regulation of Rab 5C-dependent endocytosis of cisplatin, glycolytic enzymes and vimentin, and up-regulation of antioxidant proteins, suggesting Rab 5C is a potential target for treatment of drug-resistant ovarian cancer. This constitutes a further step towards a comprehensive understanding of drug resistance in ovarian cancer.
2017-03-29 | MSV000080724 | MassIVE
Project description:Epithelial ovarian cancer (EOC) is the most lethal gynecological malignancy. On the basis of its histopathology and molecular-genomic changes ovarian cancer has been divided into subtypes, each with distinct biology and outcome. The aim of this study was to develop a panel of patient-derived EOC-xenografts that recapitulate the molecular and biological heterogeneity of human ovarian cancer. Thirty-four EOC-xenografts were successfully established, either subcutaneously or intraperitoneally, in nude mice. The xenografts were histologically similar to the corresponding patient tumor and comprised all the major ovarian cancer subtypes. After orthotopic transplantation in the bursa of the mouse ovary, they disseminate into the organs of the peritoneal cavity and produce ascites, typical of ovarian cancer. Gene expression analysis and mutation status indicated a high degree of similarity with the original patient and discriminate different subsets of xenografts. They were very responsive, responsive and resistant to cisplatin, resembling the clinical situation in ovarian cancer. This panel of patient-derived EOC-xenografts that recapitulate the recently type I and type II classification serves to study the biology of ovarian cancer, identify tumor-specific molecular markers and develop novel treatment modalities.
2015-01-07 | GSE56920 | GEO