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Prevalent p53 gain-of-function mutants co-opt epigenetic pathways to drive cancer growth

ABSTRACT: We investigated the genomewide binding pattern of prevalent p53 gain-of-function (GOF) mutants by ChIP-seq, in a panel of breast cancer cell lines. We assessed the genomewide changes of H3K4me3 upon GOF p53 knockdown in MDA-MB-468 breast cancer cells bearing the p53 R273H mutation.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE59176 | GEO | 2015/07/31

SECONDARY ACCESSION(S): PRJNA254538

REPOSITORIES: GEO

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Prevalent p53 gain-of-function mutants co-opt epigenetic pathways to drive cancer growth

Project description:We investigated the genomewide binding pattern of prevalent p53 gain-of-function (GOF) mutants by ChIP-seq, in a panel of breast cancer cell lines. We assessed the genomewide changes of H3K4me3 upon GOF p53 knockdown in MDA-MB-468 breast cancer cells bearing the p53 R273H mutation. This study uses ChIP-seq of H3K4me3 and histone H3 in wild-type or p53 R172H knock-in MEFs. Additionally, this study examines the transcriptome of wild-type or p53 R172H knock-in MEFs using polyA+ RNA-seq.

2015-07-31 | E-GEOD-59176 | biostudies-arrayexpress

Prevalent p53 gain-of-function mutants co-opt epigenetic pathways to drive cancer growth

Project description:Prevalent p53 gain-of-function mutants co-opt epigenetic pathways to drive cancer growth

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Distinct gain of function mechanism for the hot-spot mutant p53R175H

Project description:TP53 (p53) is the most commonly mutated gene in human cancers, and p53 missense mutations are present in more than 40% of all human tumors. Most p53 mutations are located within the DNA binding domain, including hotspot mutations R175H, R248W, and R273H. To elucidate the precise mechanism by which p53 missense mutants execute their gain-of-functions (GOFs) in vivo, we used a proteomic screen to identify any protein that recognizes the p53 DNA-binding domain (DBD) in a manner dependent on its mutation status. To do so, we first purified the potential binding proteins associated with the p53 DBD through multi-step affinity chromatography from a SFB-p53 H1299 stable cell line. The affinity-purified SFB-p53 interacting proteins were detected by liquid chromatography mass spectrometry/mass spectrometry (LC–MS/MS) and revealed a few cellular proteins that have been reported to interact with the DNA binding domain of p53, such as TP53BP1, USP28, and Sirt1. Interestingly, we also identified many new interacting proteins from the same complex.

2023-02-17 | PXD039886 | Pride

ChIP-chip data for identifying target genes and consensus binding sequences of mutant p53 in MDA-MB-468 breast cancer cells

Project description:The tumor suppressor p53 exerts its role mainly as a transcription factor. The TP53 gene, which encodes the p53 protein, is the most commonly mutated gene in human cancers, particularly triple negative breast cancer (TNBC). Variations in the TP53 gene occur mainly in exons 5–8 and result in missense mutations in the DNA-binding domain of the p53 protein that alter DNA binding specificity. To identify the target genes of mutant p53, we performed chromatin immunoprecipitation followed by DNA microarray (ChIP-chip). Briefly, the TNBC cell line MDA-MB-468 containing the endogenous p53-R273H mutation (the arginine residue at position 273 is mutated to a histidine) was cross-linked with 1% formaldehyde and ultrasonically sheared to generate chromatin fragments in a range of 200∼1000 bp. An aliquot of the sheared chromatin was kept as input, and the other chromatin was precipitated with a p53 monoclonal antibody. DNA was purified from the precipitated chromatin and the unprecipitated chromatin (i.e., input), amplified, and labeled with Cy5 (ChIP DNA) or Cy3 (input DNA). Cy5- and Cy3-labeled DNA samples were cohybridized with the NimbleGen Human ChIP-chip 2.1 M Deluxe Promoter Array. The raw and analyzed data are described in this article. They are useful for identifying target genes and consensus binding motifs of the p53 R273H mutant and for further clarifying the molecular mechanism underlying the oncogenic activity of the p53 mutant.

2019-12-08 | GSE128304 | GEO

Gain-of-function p53 mutants co-opt chromatin pathways to drive cancer growth.

Project description: Not available

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Gene expression profiling of MDA-MB-468 cells following p53-R273H mutant knock-down

Project description:A total of 58 genes were up-regulated (> 1.5 fold-change) while 117 genes were down-regulated Microarray experiments were performed in duplicate as follows: MDA-MB-468 cells were transduced with lentiviral shRNA targeting endogenous p53-R273H mutant (p53si-1)or a non-targeting shRNA (NS). Total RNA from cells was extracted using Qiagen RNA isolation kit (Qiagen, Valencia, CA, USA) according to the manufacturersâ protocol. RNA purity was examined by spectrophotometric determination at 260/280 nm. The microarray hybridizations were carried out using the Affymetrix Human Gene 1.0 ST arrays.

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Gain-of-Function p53 Protein Transferred via Small Extracellular Vesicles Promotes Conversion of Fibroblasts to a Cancer-Associated Phenotype

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Mutant p53 elicits context-dependent pro-tumorigenic phenotypes (ChIP-Seq)

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2021-12-23 | GSE157335 | GEO

RNA-seq of cell lines containing p53-R273H or p53-R273H 22/23

Project description:RNA-seq of cell lines containing p53-R273H or p53-R273H 22/23

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