GDF15 is a secretary protein from ovarian cancer cell A2780 and induced by cisplatin in vivo
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE122287 | GEO | 2018/11/08
REPOSITORIES: GEO
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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: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: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.
2009-04-17 | GSE15373 | GEO
Project description:The aim of this experiment was to evaluate the changes in gene expression in response to hypoxia and/or cisplatin in an ovarian cancer cell line model. A2780 (cisplatin-sensitive) and A2780cis (cisplatin-resistant) cell lines were treated with cisplatin in normoxia or hypoxia (0.5% O2) for 72 hours. RNA was extracted from three independent biological replicates for each condition: A2780 (normoxia, untreated); A2780 (hypoxia, untreated); A2780 (normoxia, cisplatin); A2780cis (hypoxia, cisplatin), A2780cis (normoxia, untreated); A2780cis (hypoxia, untreated); A2780cis (normoxia, cisplatin); A2780cis (hypoxia, cisplatin) and interrogated on Affymetrix Human Gene ST 1.0 arrays.
2016-01-15 | E-MTAB-3645 | biostudies-arrayexpress
Project description:The goal of this study was to determine genes with altered expression after selection of ovarian cancer cells for survival in increasing concentrations of cisplatin. A series of progressively cispatin resistant derivatives of A2780 ovarian cancer cell lines was hybridized to spotted cDNA microarrays using two color technology using the parental A2780 cells as a reference. Duplicate hybridizations were carried out for each resistant derivative.
2013-12-22 | E-GEOD-44022 | biostudies-arrayexpress
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:This SuperSeries is composed of the following subset Series: GSE15372: Expression data from A2780 (cisplatin-sensitive) and Round5 A2780 (cisplatin-resistant) cell lines. GSE15373: Promoter CpG island methylation data from A2780 (cisplatin-sensitive) and Round5 A2780 (cisplatin-resistant) cell lines. Refer to individual Series
2009-04-17 | E-GEOD-15709 | 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.
2013-10-25 | GSE51683 | 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: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