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Transcriptome analysis of polymorphic p53 codon 72 under genotoxic stress

ABSTRACT: Transcriptome analysis of polymorphic p53 codon 72 under genotoxic stress

PROVIDER: PRJNA761662 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15809382_1.fastq.gz	Fastqsanger.gz
	SRR15809382_2.fastq.gz	Fastqsanger.gz
	SRR15809383_1.fastq.gz	Fastqsanger.gz
	SRR15809383_2.fastq.gz	Fastqsanger.gz
	SRR15809384_1.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of polymorphic p53 codon 72 under genotoxic stress

Project description:We report the transcriptome data produced from isogenic polymorphic p53 codon 72 iPSCs under doxorubicin treatment. By inserting BAC DNA into one allele of the heterozygous polymorphic p53 codon 72, each clone expressed a p53 protein encoding P72 or R72 from another allele in which it was not inserted. The transcriptional regulation of p53 target genes was compared between the isogenic lines under doxorubicin treatment.

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The codon 72 polymorphism of p53 regulates interactions with NF-κB and transactivation of genes involoved in immunity and inflamation

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The codon 72 polymorphism of p53 regulates interactions with NF-κB and transactivation of genes involoved in immunity and inflamation

Project description:A common polymorphism at codon 72 in the p53 tumor suppressor gene encodes either proline(P72) or arginine(R72). These two variants might possess altered biological function which influences p53’s transcriptional, senescence and apoptotic functions. We found that P72 has increased apoptosis when compare to R72. To further identify unknown p53 target genes which might play a role in the increased apoptosis in P72 thymocytes, we have employed whole genome microarray expression profiling as a discovery platform. Mouse thymocytes were isolated from the thymuses of mice that were untreated (0 hour) or following 2 or 4 hours of exposure to 5 Gray of gamma radiation. Mouse thymocytes were isolated from the thymuses of mice that were untreated (0 hour) or following 2 or 4 hours of exposure to 5 Gray of gamma radiation. Four independent experiments were performed at each time point (P72 and R72) and at each timepoint 2 mice of each genotype were used, and their thymocytes were pooled together.

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Project description:Mutant forms of p53 protein often possess pro-tumorigenic function, conferring increased survival and migration to tumor cells via its “gain of function” activity. Whether and how a common polymorphism in TP53 at amino acid 72 (Pro72Arg, hereafter P72 and R72) impacts this gain of function has not been determined. We show that mutant p53 enhances migration and metastasis of tumors through the ability to bind and regulate PGC-1α, and that this regulation is markedly impacted by the codon 72 polymorphism. Tumor cells with the R72 variant of mutant p53 show increased PGC-1α function, along with greatly increased mitochondrial function and metastatic capability. Breast cancers containing mutant p53 and the R72 variant show poorer prognosis compared to P72. The combined results reveal PGC-1α as a novel “gain of function” partner of mutant p53, and indicate that the codon 72 polymorphism influences the impact of mutant p53 on metabolism and metastasis.

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