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Expression analysis of Saos-2 cells expressing p53-His273

ABSTRACT: Our compound (PRIMA) selectively kills tumor cells expressing mutant p53. Here in our study we decided to investigate the impact of our compound on the transcriptome of p53 mutant-expressing cells, Saos2-His273.

ORGANISM(S): Homo sapiens

PROVIDER: GSE15368 | GEO | 2009/04/15

SECONDARY ACCESSION(S): PRJNA123255

REPOSITORIES: GEO

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Expression analysis of Saos-2 p53-null cells

2009-04-15 | GSE15367 | GEO

Expression analysis of Saos-2 cells expressing p53-His273

Project description:Our compound (PRIMA) selectively kills tumor cells expressing mutant p53. Here in our study we decided to investigate the impact of our compound on the transcriptome of p53 mutant-expressing cells, Saos2-His273. We plated Saos-2-His273 cells and treated them with our compound for 6h or 12h. We then harvested the cells, extracted the RNA, and followed the protocol to run affymetrix array to analyse the impact of our drug on the whole transcriptome of cells expressing mutant p53.

2009-04-15 | E-GEOD-15368 | biostudies-arrayexpress

Expression analysis of Saos-2 p53-null cells

Project description:Our compound (PRIMA) selectively kills tumor cells expressing mutant p53. Here in our study we decided to investigate the impact of our compound on the transcriptome of Saos2 cells lacking p53. We plated Saos-2 cells, and treated them with our compound for 6h or 12h. We then harvested the cells, extracted the RNA, and followed the protocol to run affymetrix array to analyse the impact of our drug on the whole transcriptome of cells lacking p53.

2009-04-15 | E-GEOD-15367 | biostudies-arrayexpress

Transcription profiling of human steosarcoma cell line Saos-2 infected separately with p53 and TAp73beta expressing adenovirus to identify targets specifically regulated by TAp73

Project description:The p53 family consists of three members, p53, p73, and p63. These proteins share a high degree of amino-acid sequence similarity and major functional domains. The p53 gene, the first member of the family to be identified, is the most frequent target gene for genetic alterations in human cancers. In contrast, p73 and p63 are mainly involved in normal development and differentiation. These differences among the p53 family are likely to depend on activation or repression of different sets of target genes. In this study, to identify targets specifically regulated by p73, we performed microarray analysis and compared expression patterns in a human steosarcoma cell line Saos-2 infected separately with p53 and TAp73beta expressing adenovirus. Experiment Overall Design: Saos2 osteosarcoma cells were infected with p53, TAp73beta expressing or control adenovirus for 24 h and then harvested.

2008-11-15 | E-GEOD-13504 | biostudies-arrayexpress

Effects of PRIMA-1 treatment on Saos-2 p53-null and Saos-2 p53-His273 cells

Project description:This SuperSeries is composed of the following subset Series: GSE15367: Expression analysis of Saos-2 p53-null cells GSE15368: Expression analysis of Saos-2 cells expressing p53-His273 Refer to individual Series

2009-04-15 | E-GEOD-15658 | biostudies-arrayexpress

Genome-wide analysis of p53 binding protein

Project description:Tumor suppressor p53 regulates various role in the cell including cell cycle arrest, DNA repair and apoptosis. Current research achieved to investigate p53 target genes in human osteosarcoma cell line-SaOS2 cell. Examination of p53 binding protein by transfecting flag-tagged wild type p53 into SaOS2 cells.

2014-04-01 | E-GEOD-51268 | biostudies-arrayexpress

Variability in functional p53 reactivation by Prima-1Met/APR-246 in Ewing sarcoma

Project description:Though p53 mutations are rare in Ewing sarcoma, there is a strong indication that p53-mutant tumors form a particularly bad prognosis group. As such, novel treatment strategies are warranted that would specifically target and eradicate tumor cells containing mutant-p53 in this subset of ES patients. PRIMA-1Met/APR-246 is a small organic molecule which has been shown to restore tumor suppressor function primarily to mutant p53 and to also induce cell death in various cancer cell types.

2013-11-12 | GSE49967 | GEO

Analysis for expression of genes in multiple myeloma cells treated with PRIMA-1Met or dimethyl sulfoxide (DMSO) control

Project description:Targeting p53 by the small molecule PRIMA-1Met/APR-246 has shown promising preclinical activity in various cancer types. However, the mechanism of PRIMA-1Met-induced apoptosis is not completely understood and its effect on multiple myeloma (MM) cells is unknown. In this study we evaluated anti-tumor effect of PRIMA-1Met alone or combined with current anti-myeloma agents in MM cell lines, patient samples, and a mouse xenograft model. Results of our study showed that PRIMA-1Met decreased the viability of MM cells irrespective of p53 status with limited cytotoxicity toward normal hematopoietic cells. PRIMA-1Met restored wild type conformation of mutant p53 and induced activation of p73 up-regulating Noxa and down-regulating Mcl-1 without significant modulation of p53 level. Importantly, PRIMA-1Met delayed tumor growth and prolonged survival of mice bearing MM tumor. To identify the potential targets of PRIMA-1Met, we performed gene expression profiling (GEP) by microarray in three different cell lines harboring wild type, mutant or null p53 and analysed differential expression of target genes between PRIMA-1Met treated and non-treated samples. Based on our we conclude that treatment of MM cells with PRIMA-1Met lead to induction of p73-mediated apoptosis by up-regulating Noxa and down-regulating Mcl-1 irrespective of p53 status.

2013-05-04 | GSE46609 | GEO

Genome-wide analysis of p53 binding protein

2014-04-01 | GSE51268 | GEO

TOV112D cells treated with NSC319726

Project description:Rescuing the function of mutant p53 protein is an attractive cancer therapeutic strategy. Using the NCI anticancer drug screen data, we identified two compounds from the thiosemicarbazone family that manifest increased growth inhibitory activity in mutant p53 cells, particularly for the p53R175 mutant. Mechanistic studies reveal that NSC319726 restores WT structure and function to the p53R175 mutant. This compound kills p53R172H knock-in mice with extensive apoptosis and inhibits xenograft tumor growth in a 175-allele specific mutant p53 dependent manner. This activity depends upon the zinc ion chelating properties of the compound as well as redox changes. These data identify NSC319726 as a p53R175 mutant reactivator and as a lead compound for p53 targeted drug development. We utilized gene expression microarrays to examine the transcriptional activity of p53 targets in TOV112D cells after treatment with NSC319726.

2012-02-22 | GSE35972 | GEO

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