Comparing control and IL17A treated A2780-derived ovarian cancer stem cell
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: tong xiang
PROVIDER: E-GEOD-39698 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:A2780-derived ovarian cancer stem cells were in vitro cultured in the presence of 10 ng/mL basic fibroblast growth factor , 20 ng/mL epidermal growth factor , 5 μg/mL insulin, 0.4% bovine serum albumin. Then ovarian cancer stem cells were stimulated for 4 and 6 hours in the presence or absence of 250ng/ml IL17A. Total RNA was isolated and processed according to the Agilentmanufacturer’s standard protocols
2012-07-28 | GSE39698 | GEO
Project description:A2780 ovarian cancer cells and a cisplatin resistant derivate of A2780 cells, obtained from ECACC, UK, No. 93112519 [A2780] and No. 93112517 [A2780 cis] were seeded out in T-75 flasks at a density of 2x106 for A2780sens and 3x106 for A2780cis cells in 15 ml of medium and preincubated overnight. Medium was removed and 15 ml fresh medium (37M-0C) with different concentrations of cisplatin, liposomal cisplatin or empty liposomes were added and incubated for 72 h at 37M-0C in a 5% CO2 incubator. In case of A2780sens cells, 1.72 M-5M cisplatin (IC50 concentration) and in case of A2780cis cells 8.94 M-5M cisplatin (IC50 concentration) were added. Liposomal formulations contained equal cisplatin concentrations. Empty liposomes were added in the same concentration as the liposomal cisplatin, to analyze the impact of liposomal lipids (A2780sens: 0.80M-5mol lipid, A2780cis: 4.15 M-5mol lipid). After incubation, medium was removed and cells were washed thrice with 10 ml PBS. 1 ml RLT-buffer was added and cells lysates were stored at -80M-0C until RNA extraction.
2010-12-13 | E-MEXP-2840 | biostudies-arrayexpress
Project description:Differences in gene expression in A2780C20 vs. A2780 and A2780 treated with temsirolimus at 24-hr and 48-hr. The A2780 are human ovarian carcinoma cellls were purchased to the European Collection of Cell Cultures (ECACC). The A2780CP20 are cisplatin resisatnt cells derived of the A2780 cells. A2780CP20 cells were generated by Dr. Robert Ozols (J. Natl. Cancer Inst. 84, 264-267 (1992) by treatment of A2780 cells with incresing concentrations of cisplatin. The goal of this study is to determine whether the cisplatin and temsirolimus resistance are co-regulated. The objectives of this study are to identify additional genes differentially expressed in cisplatin sensitive and cisplatin resistant ovarain cancer cells and the changes in gene expreession upon temsirolimus treatment of A2780 cells. RNA was isolated from A2780, A2780CP20, A2780 plus temsirolimus 24-hr, and A2780 plus temsirolimus 48-hr. Labelled samples were hybridized to Affymetrix GeneChip Gene 1.0 ST Human Arrays.
2013-10-25 | E-GEOD-51683 | biostudies-arrayexpress
Project description:Transcriptional profiling of human ovarian cancer cells comparing control vehicle-treated A2780 and OVCAR-3 (Human ovarian cancer cell lines) cells with A2780 and OVCAR-3 cells treated with 5μM LS-98 for 24 hours.Goal was to determine the effects of LS-98 compound on the global A2780 and OVCAR-3 cells gene expression. One-condition experiment, control vehicle-treated A2780 and OVCAR-3 vs. LS098 treated-A2780 and OVCAR-3 cells. Biological replicates: 2 replicates.
2011-06-01 | E-GEOD-29668 | 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.
2016-07-06 | PXD001176 | Pride
Project description:SRSF3 is overexpressed in human invasive ovarian cancer and its overexpression is required for cancer cell growth and survival. To decipher the mechnisms behind the role of SRSF3 in ovarian cancer, we examined the gene expression and splicing in the ovarian cancer cell line that was engineered to express a doxycycline-induced SRSF3 siRNA, which was able to knockdown SRSF3 expression by 90% and induce apoptosis. Total RNAs extracted from A2780/SRSF3si2, a subline of ovarian cancer cell line A2780, treated with or without doxycycline at 0.1ug/ml for three days were analyzed using Affymetrix GeneChip® Human Exon 1.0 ST Array
2015-08-06 | E-GEOD-71745 | biostudies-arrayexpress
Project description:Cisplatin and carboplatin are the primary first-line therapies for the treatment of ovarian cancer. However, resistance to these platinum-based drugs occurs in the large majority of initially responsive tumors, subsequently resulting in a poor long-term prognosis. To model the onset of drug resistance, and investigate the DNA methylation alterations associated with cisplatin resistance, we treated clonally derived, drug-sensitive A2780 epithelial ovarian cancer cells with increasing concentrations of cisplatin. After several cycles of drug selection, the isogenic drug-sensitive and -resistant pairs were subjected to global CGI methylation microarray analyses. We treated clonally derived, drug-sensitive A2780 epithelial ovarian cancer cells with increasing concentrations of cisplatin. After several cycles of drug selection, the isogenic drug-sensitive and -resistant pairs were subjected to global CGI methylation analyses by differential methylation hybridization (DMH) using a customed 44K promoter CGI microarray.
2010-06-19 | E-GEOD-15373 | biostudies-arrayexpress
Project description:The identification and characterization of subpopulations of cancer stem cells (CSCs) provide new understandings and possible therapeutic implications in cancer biology. We found the ovarian cancer sphere cells possessed CSCs properties maintained self renewal, drug resistance, and tumorigenesis. Using high-throughput microarray system, we identified common GO terms and pathway signatures significantly enriched in ovarian and breast cancer stem cells. Ovarian and breast cancer cells were cultured in sphere formation conditions, and total RNA from those spheres and conresponding adhered cell was hybridized on Affymetrix microarrays.
2013-11-25 | E-GEOD-43657 | biostudies-arrayexpress
Project description:Available evidence has suggested that integrin-linked kinase (ILK) underwent over-expression in ovarian cancer while specific gene silencing of ILK resulted in apoptosis of ovarian cancer cells. Here, potential mechanisms in which ILK induces cell apoptosis was explored from the perspective of microRNA (miRNA) expression. Alteration in global miRNA expression profile was detected by miRNA microarray technique after ILK shRNA expression lentivirus was transfected into A2780 cells (n = 3). Additionally, the A2780 cells infected by scrambled shRNA lentivirus were treated as negtive control (n = 3).
2016-06-28 | E-GEOD-83721 | biostudies-arrayexpress
Project description:Cisplatin and other platinum-based drugs are widely used in the treatment of ovarian cancer, but most patients acquire the drug resistance that greatly compromises the efficacy of drugs. Understanding the mechanism of drug resistance is important for finding new therapeutic approaches. In the present study, we found that the expression of vimentin was down-regulated in drug-resistance ovarian cancer A2780-DR and SKOV-3/DDP cells compared to the drug sensitive A2780 and SKOV-3 cells. Overexpression of vimentin in A2780-DR cells markedly increased their sensitivity to cisplatin, whereas knockdown of vimentin in A2780 cells increased the resistance to cisplatin, demonstrating that vimentin plays an important role in cisplatin resistance. Quantitative proteomic analysis identified 95 differentially expressed proteins between A2780-VIM-KN and control cells, which involved in many cellular processes. Down-regulation of endocytic proteins and the up-regulation of exocytic proteins were proposed to contribute the decreased cisplatin accumulation in A2780-VIM-KN cells. Cancer stem cell markers were found to be up-regulated in A2780-VIM-KN cells which were more facile to form spheroids as compared to control cells. Our results also showed that down-regulation of vimentin increased the 14-3-3 mediated retention of Cdc25C in the cytoplasm, leading to inactivation of Cdk1 and the prolonged G2 arrest that allows the longer period of time for cells to repair cisplatin-damaged DNA. Taken together, the down-regulation of vimentin enhances cells’ resistance to cisplatin via mediating multiple cellular processes, suggesting that vimentin is a potential target for treatment of drug resistant ovarian cancer.
2018-10-24 | PXD002825 | Pride