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Sex and mutation specific p53 gain-of-function activity in gliomagenesis [RNA-seq]

ABSTRACT: Sex and mutation specific p53 gain-of-function activity in gliomagenesis [RNA-seq]

PROVIDER: PRJNA779980 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16931900_1.fastq.gz	Fastqsanger.gz
	SRR16931900_2.fastq.gz	Fastqsanger.gz
	SRR16931901_1.fastq.gz	Fastqsanger.gz
	SRR16931901_2.fastq.gz	Fastqsanger.gz
	SRR16931902_1.fastq.gz	Fastqsanger.gz

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Sex and mutation specific p53 gain-of-function activity in gliomagenesis

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Sex and mutation specific p53 gain-of-function activity in gliomagenesis [RNA-seq]

Project description:The goal of this study is to compare the sex specific effects of the expression of p53 missense mutations on the transcriptomes of male and female primary astrocytes. Primary cortical astrocytes harboring a single floxed Trp53 allele were harvested from male and female postnatal day one pups, and transduced with mutant p53;IRES GFP followed by CRE recombinase. mRNA was collected from male and female astrocytes transduce with mouse Trp53:R172H, Trp53:Y202C, or Trp53:Y217C. This study revealed sex specific gain-of-function effects on the transcriptomes of each cell line that correlated with cancer pathways.

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Project description:ChIP-seq analysis of Primary cortical astrocytes harboring a single floxed Trp53 allele harvested from male and female postnatal day one pups, and transduced with mutant p53;IRES GFP followed by CRE recombinase. p53 protein was immunoprecipated from fixed whole chromatin from cells expressing one of three mutants or p53 KO control.

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Sex and mutation specific p53 gain-of-function activity in gliomagenesis

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Project description:We have identified a relatively rare mutation in p53 in an Indian oral cancer patient sample at the fade end of its DNA binding domain [P152L]. Although P152L p53 DBD potentially binds to DNA, the full length protein is completely devoid of cognate site DNA binding ability. Also the mutant protein can efficiently tetramerize. Significantly, this mutant was found to induce cell mobility and proliferation with greater tumorigenic potential in nude mice, the mechanistic details of which is also investigated upon. These data establish P152L as a new gain of function p53 mutation

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Project description:Mutant p53 proteins, resulting form frequent TP53 tumor suppressor missense mutations, possess gain-of-function activities and are among the most widespread and robust oncoproteins in human tumors. They are potentially important but understudied therapeutic targets. No studies to date have distinguished common, therapeutically relevant mutant p53 gain-of-function effects, from effects specific to different mutant variants and cell backgrounds. Here we identify 26S proteasome machinery as the common downstream effector controlled by mutant p53s in Triple Negative Breast Cancer (TNBC - aggressive carcinomas with TP53 as the most frequently mutated locus) and conserved in other human cancers. We have identified this pathway using a combination of single-model, multi-method vertical analysis (whole cell proteome, RNA sequencing an ChIP sequencing) and multi-cell line, horizontal analysis of transcriptiomes. We found that different missense mutant p53s regardless of the cell background transcriptionaly activate whole 26S proteasome machinery. Proteasome activity is significantly increased in p53 mutant versus wild-type or knockdown/null status - in cellular and mouse models as well as in human breast tumors. Increased proteasome activity leads to inhibition of tumor suppressive pathways. The control of mutant p53 over proteasome transcription and activity results in the increased resistance to proteasome inhibitors. By combining the mutant p53 targeting agents and proteasome inhibitor we were able to overcome the “bounce-back” proteasome inhibitor resistance mechanism in mutant p53 bearing TNBC cells and xenografts in vivo.

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