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TOV112D cells treated with NSC319726

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE35972 | GEO | 2012/02/22

SECONDARY ACCESSION(S): PRJNA151623

REPOSITORIES: GEO

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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. Triplicate cultures of TOV112D cells untreated, treated with NSC319726. Total RNA was extracted and hybridized to Affymetrix human U133 plus 2.0 microarrays.

2012-02-22 | E-GEOD-35972 | biostudies-arrayexpress

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

Expression analysis of Saos-2 cells expressing p53-His273

2009-04-15 | GSE15368 | GEO

Expression analysis of Saos-2 p53-null cells

2009-04-15 | GSE15367 | GEO

Unique Transcriptional Profiles Underlie Osteosarcomagenesis Driven by Different p53 Mutants (RNA-Seq)

Project description:To identify mutant p53 GOF, murine primary osteosarcomas expressing p53R172H or p53R245W over null and p53-null osteosarcomas were processed for bulk sequencing; DEGs were identified in p53R172H and p53R245W expressing tumors by comparing to p53-null tumors; DEGs were used to identify dysregulated pathways and mutant p53 GOF

2023-05-12 | GSE231849 | GEO

Mouse oral tumors induced by activation of Ras and p53 mutations

Project description:The p53 gain of function p53R172H promotes accelerated tumor growth and progression to carcinoma. To identify gene expression changes associated with the oncogenic function of mutant p53 we compared the expression profiles of oral tumors induced by activation of oncogenic K-ras and p53 gain- or loss-of-function mutations Oral tumors were induced by activation of endogenous oncogenic K-rasG12D and p53 loss- or gain-of-function mutations (p53R172H) Oral tumors from mice carrying the p53R172H mutation or deletion of p53 were collected for gene expression analysis

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Mouse oral tumors induced by activation of Ras and p53 mutations

2012-03-31 | GSE28203 | GEO

Expression data from salivary tumor tissues derived from MMTV-ras transgenic mice with wild-type p53, no p53 or gain-of-function mutant p53

2014-08-15 | GSE59452 | GEO

Expression data from salivary tumor tissues derived from MMTV-ras transgenic mice with wild-type p53, no p53 or gain-of-function mutant p53

Project description:Salivary tumors isolated from MMTV-ras transgenic mice expressing wild-type p53, no p53 or p53R172H gain-of-funcion mutant were subjected to genome-wide gene expression profiling to assess the effect of the different p53 status on tumor gene expression. A total of 12 spontaneous salivary tumors from MMTV-ras/p53+/+, MMTV-ras/p53-/- or MMTV-ras/p53R172H/R172H mice (4 tumors per genotype) were analyzed using Affymetric GeneChip for gene expression profiling. The multi-class comparison function of Significance Analysis of Microarray (SAM) with an FDR of 1% was used to identify genes that are differentially regulated across the three genotypic groups.

2014-08-15 | E-GEOD-59452 | biostudies-arrayexpress

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