High-throughout sequencing of ovarian cancer cells treated with Annonacin and Carboplation
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE283821 | GEO | 2024/12/14
REPOSITORIES: GEO
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Project description:The high-throughput sequencing technology was performed after the treatment of human ovarian cancer cells A2780 with TMPyP4 and H2O2 purchased from Sigma-Aldrich, to explore the expression of genes related to cell proliferation, DNA damage and ROS levels of ovarian cancer cells A2780 after the treatment of TMPyP4 and H2O2, and to find an interesting target pathway,HIF-1 signaling pathway.
2024-03-25 | GSE262015 | GEO
Project description:To investigate the function of Luteolin and siVRK1 on ovarian cancer, we use A2780 and ES2 cell lines treated with siCtrl, siVRK1, DMSO and luteolin to do the experiment. We then performed gene expression profiling analysis using data obtained from RNA-seq .
2022-09-07 | GSE212598 | GEO
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.
2013-10-25 | GSE51683 | GEO
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: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: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: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
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, we measured gene expression alterations associated with cisplatin resistance. We treated clonally derived, drug-sensitive A2780 epithelial ovarian cancer cells with increasing concentrations of cisplatin. After 5 cycles of drug selection, the isogenic drug-sensitive (parental A2780) and -resistant (Round5 A2780) cell lines were subjected to mRNA expression microarray analyses.
2009-04-17 | E-GEOD-15372 | 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.
2011-06-01 | GSE29668 | GEO
Project description:We provide a series of chromatin and transcriptomic profiles to establish the short-term and long-term effects of cisplatin treatment in ovarian cancer A2780 cells.
2020-04-01 | GSE129701 | GEO