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Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 3]

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE143691 | GEO | 2020/04/01

REPOSITORIES: GEO

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Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 2]

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

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 1]

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 | GSE129700 | GEO

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-04-01 | GSE129702 | GEO

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 2]

Project description:Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 2]

| PRJNA532532 | ENA

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 1]

Project description:Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 1]

| PRJNA532531 | ENA

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 3]

Project description:Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 3]

| PRJNA601312 | ENA

Down-regulation of Vimentin Increased Drug Resistance in Ovarian Cancer Cells

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

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells

Project description:Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells

| PRJNA532526 | ENA

Expression data from A2780 (cisplatin-sensitive) and Round5 A2780 (cisplatin-resistant) cell lines.

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

Ovarian cancer cell line LC-MS-MS

Project description:A2780-DR cells are cisplatin resistance compared to A2780. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. To demonstrate how H19 contributes to cisplatin-resistance in ovarian cancer, proteomic analysis was carried out on A2780, A2780-DR, A2780-DR/H19si, and A2780-DR/control cells. Proteins expression levels were identified and quantified using MaxQuant software (http://medusa.biochem.mpg.de/maxquant_doku/). The experiments were repeated twice and the false-positive rate was set to be <1%. Based on label-free quantification intensity ratios (>1.67 or <0.6) in proteins that have two or more unique peptides.

2018-10-25 | PXD003252 | Pride

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