Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA194571 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Characterization of differential gene expression due to cisplatin resistance in human ovarian cancer spheroids by microarray analysis. In this dataset, we include the expression data obtained from cisplatin-sensitive and cisplatin-resistant human ovarian cancer spheroids. These data are used to obtain 1316 genes that are differentially expressed in response to cisplatin resistance.
2015-12-01 | GSE45553 | GEO
Project description:Collagen type XI alpha 1 (COL11A1) is identified as one of the most upregulated genes in cisplatin-resistant ovarian cancer and recurrent ovarian cancer. However, the exact functions of COL11A1 in cisplatin resistance are unknown. The goal of this study is to determine molecular mechanisms by which COL11A1 confers cisplatin resistance in ovarian cancer cells. We overexpressed COL11A1 in A2780 and OVCAR3 ovarian cancer cells, which express very low endogenous levels of COL11A1. We then compared the mRNA expression levels of various genes between COL11A1-overexpressing ovarian cancer cells and control ovarian cancer cells by RNA-Seq. Our RNA-Seq data show that COL11A1 overexpression did not consistently change the expression levels of genes involved in cisplatin efflux, glutathione metabolism, and DNA repair pathways, which are known to contribute to cisplatin resistance. This result implies that COL11A1 might confer cisplatin resistance in ovarian cancer cells through other mechanisms.
2019-10-10 | GSE112985 | GEO
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:Molecular mechanisms underlying the development of resistance to platinum treatment in patients with ovarian cancer remain poorly understood. This is mainly due to the lack of appropriate in vivo models allowing identification of factors that are regulated during initial treatment and of acquired resistance-related genes. In this study, we used whole genome microarrays and linear model analysis to identify potential resistance-related genes by comparing the expression profiles of the parental human ovarian cancer model A2780 and its cisplatin-resistant variant A2780cis, before and after carboplatin treatment in vivo.
2013-10-01 | E-MTAB-1858 | biostudies-arrayexpress
Project description:Cisplatin-resistance is a major cause of treatment failure in human ovarian cancer. Besides lots of genes involved, emerging evidences demonstrate that miRNAs contribute to cisplatin-resistance in cancer. We measured the miRNA expression profiles of cisplatin-resistant C13K ovarian cancer cell line compared with its cisplatin-sensitive OV2008 parent cell line using miRNA microarrays.
2018-09-28 | GSE120256 | GEO
Project description:Chemo-resistance to platinum such as cisplatin is critical in the treatment of ovarian cancer. Recent evidences have linked epithelial-mesenchymal transition (EMT) with the drug resistance as a contributing mechanism. The current study explored the connection between cellular responses to cisplatin with EMT in ovarian cancer. 46 ovarian carcinoma cell lines expression data with and without Cisplatin treatment.
2014-07-29 | E-GEOD-47856 | biostudies-arrayexpress
Project description:Cisplatin, a utilized anticancer drug in clinical practice, induces sensorineural hearing loss (SNHL) in patients. However, the precise mechanism underlying cisplatin-associated ototoxicity remains unknown. HEI-OC1 cells are immortalized cells derived from the organs of Corti mice and nuclear factor erythroid 2-related factor 2 （Nrf2） knockout (KO) significantly enhances cisplatin resistance in these cells. The exploration of transcriptomic data from Nrf2 KO has significant implications for the identification of novel targets to enhance HEI-OC1 cisplatin resistance in Nrf2 KO and for understanding the biological characteristics associated with SNHL. The RNA-seq analysis revealed a significant enrichment of differentially expressed genes (DEGs) in the Nrf2 KO model within key signaling pathways, including the PI3K-Akt, MAPK, as well as Glutathione metabolism signaling pathways. Notably, expression levels of 17 specific genes were confirmed by RT-qPCR (Real-time Quantitative-PCR). The biomarkers identified in this study may be key to understanding the biological mechanism by which Nrf2 KO strongly increases HEI-OC1 cisplatin resistance, and by targeting the PI3K-Akt, MAPK, Glutathione metabolism signaling pathways provide new ideas for the prevention and treatment of cisplatin-induced SNHL.
2024-09-01 | GSE268900 | GEO
Project description:Multiple DNA methylation changes have been associated with the acquisition of drug resistance; however it remains uncertain how many of these changes may represent critical DNA methylation drivers of chemoresistance. Using genome-wide DNA methylation profiling across 27,578 CpG sites on Illumina HumanMethylation27 bead array we identified loci at 4092 genes becoming hypermethylated in the chemoresistant A2780/cp70 ovarian tumour cell line compared to the parental sensitive A2780 line. Hypermethylation at CpG islands (CGI) is often associated with transcriptional silencing, however only 245 of these hypermethylated genes become down-regulated in A2780/cp70 as measured by microarray expression profiling. Treatment with the demethylating agent Decitabine induces re-sensitisation to cisplatin and resulted in re-expression of 41 of the down-regulated genes in cisplatin-resistant cells at the time point when re-sensitisation occurs. 13 of the 41 genes were consistently hypermethylated in two further independent cisplatin-resistant A2780 cell derivatives. Nine out of the 13 genes (ARHGDIB, ARMCX2, COL1A, FLNA, FLNC, MEST, MLH1, NTS, PSMB9) acquired methylation at CpG sites in ovarian tumours at relapse following chemotherapy or chemoresistant cell lines derived at the time of patient relapse. Furthermore, 5/13 candidate genes acquired methylation in drug-resistant in vivo-derived ovarian cancer sustaining (side population) cells. Therefore, this small set of genes are potential key drivers of chemoresistance and should be further evaluated as predictive biomarkers, both to existing chemotherapies, but also to epigenetic therapies used to modulate drug resistance. Array-based methylation profiling was performed using the Infinium HumanMethylation27 BeadChip in two cisplatin sensitive cell lines and three cisplatin resistant cell lines derived in vitro, four pairs of cisplatin sensitive and resistant cell lines derived in vivo, 7 pairs of tumour tissues obtained from patients before chemotherapy and at disease relapse, 2 pairs of IGROV1 SP and NSP cells. The reproducibility of the Infinium HumanMethylation27 BeadChips was evaluated using biological and technical replicates of matched chemosensitive/chemoresistant ovarian cancer cell lines PEO1/PEO4. Differential methylation cutoff was estimated from two biological replicates by bootstrap resampling.
2011-12-20 | E-GEOD-28647 | 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