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Gene expression profile associated with a cytostatic does of mifepristone in ovarian cancer cells by microarray analysis

ABSTRACT: Goal of the experiment: To examine differential gene expression in three ovarian cancer cell lines in the absence and presence of mifepristone. Brief description of the experiment: Hypothesis: The gene expression profile associated with a cytostatic response to Mifepristone will be similar between ovarian cancer cells regardless of their p53 status or sensitivity to Cisplatin. Aim: Evaluate the modifications in gene expression profile in ovarian cancer cells in response to a cytostatic concentration of Mifepristone against those in logarithmic phase of growth (Vehicle). Compare the gene expression profile of cells with different genetic backgrounds as well as between those with identical genetic backgrounds but different sensitivities to Cisplatin. Cell Types: SKOV-3 as null p53 and semi-resistant to Cisplatin, OV2008 cells as wild type p53 and hyper-sensitive to Cisplatin , OV2008/C13 cells as wild type p53 and resistant to Cisplatin. Conditions: Cells from three different passages were cultured in T25 flasks. The starting number of cells was 250,000 or 500,000, however cells were left to grow for 48 hr or 24 hr respectively before to start the treatment with Mifepristone 8.6 µg/ml (20 µM) or DMSO (vehicle) for 24 hr.

ORGANISM(S): Homo sapiens

PROVIDER: GSE29763 | GEO | 2016/06/09

SECONDARY ACCESSION(S): PRJNA141027

REPOSITORIES: GEO

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Homo sapiens

Project description:Gene expression profile associated with a cytostatic does of mifepristone in ovarian cancer cells by microarray analysis

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Differences in gene expression in A2780C20 vs. A2780

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Project description:Ovarian cancer IGROV1 cells were studied to profile the expression of wild type (WT, Cisplatin Susceptible) cells and Cisplatin Resistant (CR) cells. The goal was to gain insights or to build hypotheses into the mechanisms of Cisplatin resistance in this cell-based model.

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Targeting polyploid giant cancer cells potentiates a therapeutic response and overcomes resistance to PARP inhibitors in ovarian cancer

Project description:PARP inhibitor olaparib induces the formation of polyploid giant cancer cells (PGCCs) in ovarian and breast cancer cell lines, human high-grade serous ovarian cancer (HGSC)–derived organoids, and HGSC patient-derived xenografts (PDXs). Time-lapse tracking of ovarian cancer cells revealed that PGCCs primarily developed from endoreplication of cancer cells after exposure to sublethal concentrations of olaparib. PGCCs exhibited features of senescent cells but, after olaparib withdrawal, could escape senescence via restitutional multipolar endomitosis and other modes of cell division to generate mitotically competent resistant daughter cells. The contraceptive drug mifepristone blocked PGCC formation and daughter cell production. Mifepristone/olaparib combination therapy substantially reduced tumor growth in PDX models without previous olaparib exposure, while mifepristone alone decreased tumor growth in PDX models with acquired olaparib resistance. Thus, targeting PGCCs may represent a promising approach to potentiate the therapeutic response to PARPi and overcome PARPi-induced resistance.

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