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Expression profiling of cisplatin resistant derivatives of ovarian cancer cell line A2780

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE44022 | GEO | 2013/12/22

SECONDARY ACCESSION(S): PRJNA188568

REPOSITORIES: GEO

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Expression profiling of cisplatin resistant derivatives of ovarian cancer cell line A2780

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

Promoter CpG island methylation 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, 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

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

2009-04-17 | E-GEOD-15372 | biostudies-arrayexpress

Promoter CpG island methylation data from A2780 (cisplatin-sensitive) and Round5 A2780 (cisplatin-resistant) cell lines.

2009-04-17 | GSE15373 | GEO

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

2009-04-17 | GSE15372 | GEO

Transcription profiling by array of human A2780 ovarianc cancer cells and cisplatin resistant derivate cells treated with cisplatin or liposomal cisplatin

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

Transcription profiling of xenografted tumors derived from human ovarian cell line model A2780 and its cisplatin resistant variant A2780cis

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

Methylation profiling of cisplatin-sensitive and cisplatin-resistant human ovarian cancer cell lines

Project description:Analysis of differences in DNA methylation in cisplatin-sensitive and cisplatin-resistant ovarian cancer cell lines.

2008-01-11 | E-TABM-210 | biostudies-arrayexpress

GDF15 is a secretary protein from ovarian cancer cell A2780 and induced by cisplatin in vivo

Project description:A2780 is a cisplatin sensitive ovarian cancer cell line. A2780 ovarian cancer cells was treated with different doses of cisplatin in an attempt to identify biomarkers that can be used to predict chemoresponse. We used microarrays to identify genes induced by cisplatin in a time dependent manner.

2018-11-08 | GSE122287 | GEO

Targeting z-Crystallin by aspirin restores the sensitivity to cisplatin in resistant A2780 ovarian cancer cells

Project description:Ovarian cancer is the deadliest gynaecologic malignancies worldwide. Platinum based chemotherapy is the mainstay treatment for ovarian cancer; however, frequent recurrence and chemoresistance onset in patients with advanced diseases remain a therapeutic challenge. Although mechanisms underlying the development of chemoresistance are still ambiguous, the B-cell lymphoma-2 (Bcl-2) family is closely associated with chemoresistance in ovarian cancer. We previously disclosed that Zeta-Crystallin (CryZ) is a post-transcriptional regulator of Bcl-2 gene expression, by binding to Bcl-2 mRNA and increasing its half-life. Here, we investigated the role of CryZ as a novel therapeutic target in A2780 ovarian carcinoma cells by modulating the protein activity with acetylsalicylic acid (ASA) to restore chemosensitivity. Molecular docking and fragment-mapping based approach revealed potential interaction of ASA within CryZ protein. Inhibition of CryZ binding activity to Bcl-2 and Bcl-xl mRNA targets by ASA was demonstrated in A375 cells. Cytotoxicity assays were conducted in A2780S and A2780R ovarian cancer cells to evaluate if CryZ binding activity inhibition and CryZ silencing were able to reverse cisplatin resistance. ASA-treatment determined a downregulation of Bcl-2 and Bcl-xl mRNA levels in A2780S and A2780R cells. ASA-treatment or CryZ silencing were able to increase and restore the chemosensitivity in both sensitive and resistant A2780 ovarian cancer cells, respectively. In this research article we demonstrated that the pharmacological or genetic inhibition of CryZ restores the sensitivity to cisplatin in a model of sensitive or resistant ovarian cancer cells. These findings suggest a new gene-targeted chemotherapeutic approach to restore the cytotoxicity in drug-resistant ovarian cancers and increase the sensitivity in non-resistant cells.

2024-06-17 | GSE270030 | GEO

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