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Exon Array Expression Profiling of HCT116 (p53null) cells transfected with wildtype p53 and 6 p53 mutants

ABSTRACT: The tumor suppressor protein p53 functions to regulate diverse cellular processes including apoptosis, cell cycle, senescence and metabolism. Act as a master transcription factor, it can transcriptionally regulate the gene expression of many downstream target genes. p53 is frequently mutated in cancer by single nucleotide/amino acid substitutions at the DNA binding domain that result in a mutant form of p53 protein and usually loses its DNA binding and transcriptional regulation abilities. In this study, we performed gene expression analysis using Affymetrix Exon Array ST1.0 platform to assess the transcriptome of wildtype p53 and 6 loss-of-function p53 mutants in p53null HCT116 cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE49046 | GEO | 2013/08/19

SECONDARY ACCESSION(S): PRJNA212754

REPOSITORIES: GEO

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Exon Array Expression Profiling of HCT116 (p53null) cells transfected with wildtype p53 and 6 p53 mutants

Project description:The tumor suppressor protein p53 functions to regulate diverse cellular processes including apoptosis, cell cycle, senescence and metabolism. Act as a master transcription factor, it can transcriptionally regulate the gene expression of many downstream target genes. p53 is frequently mutated in cancer by single nucleotide/amino acid substitutions at the DNA binding domain that result in a mutant form of p53 protein and usually loses its DNA binding and transcriptional regulation abilities. In this study, we performed gene expression analysis using Affymetrix Exon Array ST1.0 platform to assess the transcriptome of wildtype p53 and 6 loss-of-function p53 mutants in p53null HCT116 cells. 8 samples were analyzed as a group. pcDNA3.1 empty construct was served as a control experiment.

2013-08-19 | E-GEOD-49046 | biostudies-arrayexpress

Influenza virus facilitates its infectivity by activating p53 to inhibit the expression of interferon-induced transmembrane proteins (IFITMs)

Project description:Transcriptome analysis of mock or H1N1 IAV PR8 infected p53WT A549 and p53null A549-KO3 cells by Affymetrix GeneChip Human Transcriptome 2.0 Arrays to achieve a set of genes those are regulated by p53 and responsive to IAV infection. Influenza A virus infection activates cellular p53, however it has not been clear whether this process has pro- or anti- viral effects. In this study, using human isogenic p53 wildtype A549 cells and p53null A549-KO3 cells generated from the CRISPR/Cas9 technology, we report that p53null cells exhibit significantly reduced viral propagation property when infected with influenza A virus (H1N1/A/Puerto Rico/8/34). Here, using genome-wide microarray analysis we revealed that p53 regulates the expression of a large set of interferon-inducible genes, some of which are directly associated with viral infectivity and later experimentally validated to be responsible for p53-regulated IAV infectivity.

2018-05-31 | GSE106279 | GEO

Gene expression profiling of E1A;HrasG12V mouse embryonic fibroblasts grown under physiological (5%) oxygen conditions, with wild-type p53 or p53 null

Project description:To investigate how pleiotropic the impact of p53 loss is on cellular function, generated isogenic, polyclonal wild-type (sgNTC) and p53-null (sgp53) E1A;HrasG12V mouse embryonic fibroblast cell lines using CRISPR/Cas9. Here we show gene expression analysis on p53 wild-type (sgNTC) and p53null (sgp53) E1A;HrasG12V MEFs grown under physiological oxygen conditions (5% oxygen).

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DBC1 regulates p53 stability via inhibition of CBP-dependent p53 polyubiquitination

Project description:The control of p53 protein stability is critical to its tumor suppressor functions. The CREB Binding Protein (CBP) transcriptional coactivator co-operates with MDM2 to maintain normally low physiologic p53 levels in cells via an exclusively cytoplasmic ‘E4’ polyubiquitination activity. Utilizing mass spectrometry to identify nuclear and cytoplasmic CBP interacting proteins that regulate compartmentalized CBP E4 activity, we identified Deleted in Breast Cancer 1 (DBC1) as a stoichiometric CBP-interacting protein that negatively regulates CBP–dependent p53 polyubiquitination, stabilizes p53, and augments p53-dependent apoptosis. TCGA analysis demonstrated that solid tumors often retain wild type p53 alleles in conjunction with DBC1 loss, supporting the hypothesis that DBC1 is selected for disruption during carcinogenesis as a surrogate for p53 functional loss. As DBC1 maintains p53 stability in the nucleus where p53 exerts its tumor suppressive transcriptional function, replacement of DBC1 functionality in DBC1-deleted tumors might also enhance p53 function and chemosensitivity for therapeutic benefit.

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Phosphorylation of p53 Serine 46 contributes to target gene selectivity of p53 (Exon)

Project description:The tumor suppressor p53 plays a crucial role in cellular growth control inducing a plethora of cellular response pathways. The molecular mechanisms that discriminate between the distinct p53-responses towards different stress treatments have remained largely elusive. Here, we have analyzed the p53-regulated pathways induced by two chemotherapeutical treatments, Actinomycin D inducing growth arrest and Etoposide resulting in apoptosis. We found that the genome-wide p53-binding patterns are almost identical upon both treatments notwithstanding transcriptional differences that we observed in genome-wide transcriptome analysis. To assess the role of post-translational modifications in target gene choice and activation we investigated the extent of phosphorylation of Serine 46 of p53 bound to DNA (p53-pS46), a modification that has been linked to apoptosis-pathways, and the extent of phosphorylation of Serine 15 (p53-pS15), a general p53-activation mark. Interestingly, the overall extent of S46 phosphorylation of p53 bound to DNA is considerably higher in cells directed towards apoptosis while the degree of phosphorylation at S15 of DNA bound p53 remains highly similar upon both treatments. Moreover, our data suggest that, following different chemotherapeutical treatments, the extent of chromatin-associated p53 phosphorylated at S46 but not at pS15 is higher on certain apoptosis related target genes, including the BAX and PUMA genes. These data provide evidence that cell fate decisions are not made primarily on the level of general p53 DNA-binding, but possibly through post-translational modifications of chromatin bound p53.

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Phosphorylation of p53 Serine 46 contributes to target gene selectivity of p53 (Exon)

2011-03-23 | E-GEOD-22184 | biostudies-arrayexpress

Pyrimidine Triones as Potential Activators of p53 Mutants

Project description:p53 is a crucial tumor suppressor in vertebrates that is frequently mutated in human cancers. Most mutations are missense mutations that render p53 inactive in suppressing tumor initiation and progression. Developing small molecule drugs to convert mutant p53 into an active, wild-type-like conformation is a significant focus for personalized cancer therapy. Prior research indicates that reactivating p53 suppresses cancer cell proliferation and tumor growth in animal models. Early clinical evidence with a compound selectively targeting p53 mutants with substitutions of tyrosine 220 suggests potential therapeutic benefits of reactivating p53 in patients. This study identifies and examines the UCI-1001 compound series as a potential corrector for several p53 mutations. The findings indicate that UCI-1001 treatment in p53 mutant cancer cell lines inhibits growth and reinstates wild-type p53 activities, including DNA binding, target gene activation, and induction of cell death. Cellular thermal shift assays, conformation-specific immunofluorescence staining, and differential scanning fluorometry suggest that UCI-1001 interacts with and alters the conformation of mutant p53 in cancer cells. These initial results identify pyrimidine trione derivatives of the UCI-1001 series as candidates for p53 corrector drug development.

2024-08-05 | GSE273169 | GEO

Gene expression signatures in HuH7 cells transfected with super hybrid p53 version 2.

Project description:The p53 tumor suppressor belongs to a gene family that includes two other structurally and functionally related members: p63 and p73. However, the regulation of p53 activity differs significantly from that of p73 and p63. To enhance the tumor suppressive activity of p53, we created a p63/p53 hybrid molecule, named p63-53O, which comprises the transcriptional activation and DNA-binding domains of TAp63γ and the oligomerization domain of p53. In this study, we generated a series of p63-53O derivatives and developed an advanced hybrid molecule named “Super Hybrid p53 (SHp53).” SHp53 efficiently transactivated several proapoptotic genes, including CASP10, KCNK3, and PYCARD, compared with p53. Moreover, the silencing of these proapoptotic genes partially abolished the apoptotic response to SHp53 in human cancer cells. The potency of SHp53 for suppressing tumorigenesis was also evaluated using in vivo models. Thus, our results identify a better p63/p53 hybrid molecule for the development of anti-cancer therapies.

2013-05-23 | GSE42493 | GEO

Transcription profiling of human H1299 cells and Saos-2 cells (p53 null cells) transfected with Flag vector, Flag-p53 WT or Flag-p53 SA

Project description:H1299 cells and Saos-2 cells (p53 null cells) were transfected with Flag vector, Flag-p53 WT or Flag-p53 SA.

2010-10-14 | E-MEXP-2556 | biostudies-arrayexpress

Gene expression signatures in HuH7 cells transfected with super hybrid p53 version 2.

Project description:The p53 tumor suppressor belongs to a gene family that includes two other structurally and functionally related members: p63 and p73. However, the regulation of p53 activity differs significantly from that of p73 and p63. To enhance the tumor suppressive activity of p53, we created a p63/p53 hybrid molecule, named p63-53O, which comprises the transcriptional activation and DNA-binding domains of TAp63? and the oligomerization domain of p53. In this study, we generated a series of p63-53O derivatives and developed an advanced hybrid molecule named “Super Hybrid p53 (SHp53).” SHp53 efficiently transactivated several proapoptotic genes, including CASP10, KCNK3, and PYCARD, compared with p53. Moreover, the silencing of these proapoptotic genes partially abolished the apoptotic response to SHp53 in human cancer cells. The potency of SHp53 for suppressing tumorigenesis was also evaluated using in vivo models. Thus, our results identify a better p63/p53 hybrid molecule for the development of anti-cancer therapies. HuH-7 human hepatocellular carcinoma cells were either transduced with adenoviral vectors expressing p53, TAp63gamma, p53-p63 hybrid (super hybrid p53 version 2, p63-53O-FL), or lacZ. After 24 hours, total RNA was isolated and analyzed by hybridization to Agilent-028004 SurePrint G3 Human GE 8x60K Microarray.

2013-05-23 | E-GEOD-42493 | biostudies-arrayexpress

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