Similar Datasets
Project description:We conducted gene expression analysis from total tumor treated with AAV-Control or AAV-mut-p53 deleted in an acute setting.
2024-01-01 | GSE213823 | GEO
Project description:Transcriptional profiling of H1299 non-small cell lung carcinoma cells transfected with either wt p53 or mut(175) p53 driven by the 5xHRE promoter (5 repeats of hypoxia-inducible factor response elements) and treated for 16 h with normoxia (21% O2) or hypoxia(<0.1% O2). 5xHRE promoter ensures that p53 expression is induced in hypoxic conditions only. Goal was to determine the transcriptional response of p53 in hypoxia and the 175 p53 mutant was used as a control as it is DNA-binding defective and transcription-incompetent mutant. Four-condition experiment: wt p53-transfected H1299 cells treated with normoxia, mut p53-transfected H1299 cells treated with normoxia, wt p53-transfected H1299 cells treated with hypoxia, mut p53-transfected H1299 cells treated with hypoxia. Biological replicates: 1 normoxic sample with wt p53, 1 normoxic sample with mut p53, 3 hypoxic samples with wt p53, 3 hypoxic samples with mut p53.
2014-01-08 | E-GEOD-53893 | biostudies-arrayexpress
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.
2019-11-13 | PXD012673 | Pride
Project description:1) Background: TP53 gene mutations occur in 70% of oesophageal adenocarcinomas (OACs). Given the central role of p53 in controlling cellular response to therapy we investigated the role of mutant (mut-) p53 and SLC7A11 in a CRISPR-mediated JH-EsoAd1 TP53 knockout model. (2) Methods: Response to 2 Gy irradiation, cisplatin, 5-FU, 4-hydroxytamoxifen and endoxifen was assessed, followed by a TaqMan OpenArray qPCR screening for differences in miRNA expression. (3) Results: Knockout of mut-p53 resulted in increased chemo- and radioresistance (2 Gy survival fraction: 38% vs. 56%, p<0.0001) and in altered miRNA expression levels. Target mRNA pathways analyses indicated several potential mechanisms of treatment resistance. SLC7A11 knockdown restored radiosensitivity (2 Gy SF: 46% vs. 73%; p=0.0239), possibly via enhanced sensitivity to oxidative stress. Pathway analysis of the predicted mRNA targets of differentially expressed miRNAs indicated potential involvement in several pathways associated with apoptosis, ribosomes as well as in p53 signalling pathways. (4) Discussion: These results provide a better understanding of the important role of SLC7A11 in cancer metabolism and redox balance and the influence of p53 on these processes. Inhibition of the SLC7A11-gluthatione axis may represent a promising approach to overcome resistance associated with mut-p53.
2021-05-31 | GSE171965 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-08-18 | GSE213824 | GEO
Project description:Proteome of exosomes purified from H1299-p53R273H (mutant) and H1299-p53-/- cells, which found the levels of Podocalyxin altered in p53-mutant cells.
2018-12-04 | PXD011241 | Pride
Project description:Transcriptional profiling of H1299 non-small cell lung carcinoma cells transfected with either wt p53 or mut(175) p53 driven by the 5xHRE promoter (5 repeats of hypoxia-inducible factor response elements) and treated for 16 h with normoxia (21% O2) or hypoxia(<0.1% O2). 5xHRE promoter ensures that p53 expression is induced in hypoxic conditions only. Goal was to determine the transcriptional response of p53 in hypoxia and the 175 p53 mutant was used as a control as it is DNA-binding defective and transcription-incompetent mutant.
2014-01-08 | GSE53893 | GEO
Project description:Loss of the p53-inducible LINC01021 in p53-proficient CRC cell lines results in increased sensitivity to DNA-damaging chemotherapeutics. Here, we comprehensively analyzed how LINC01021 affects the p53-induced transcriptional program. Using a CRISPR/Cas9-approach we deleted the p53 binding site in the LINC01021 promoter of SW480 colorectal cancer cells and subjected them to RNA-Seq analysis after activation of ectopic p53. RNA affinity purification followed by mass spectrometry was used identify proteins associated with LINC01021.
2024-05-10 | PXD050892 | Pride
Project description:Tumor associated mutant p53 proteins often gain new functions for tumorigenesis and tumor progression. It has been shown that mutant p53 can transcriptionally regulate a group of genes, which in turn contributes to mutant p53 gain of function. A mutant p53 interacting protein Pontin binds to mutant p53 and promotes its gain of function. This experiment tests whether the interaction of Pontin with mutant p53 regulates the transcriptional activity of mutant p53. We used a breast cancer cell line containing endogenous mutant p53 (SK-BR-3) with or without knockdown of mutant p53 by shRNA to identify genes regulated by mutant p53. We then knocked down endogenous Pontin in SK-BR-3 cells, and compared the transcriptional levels of these genes in cells with and without mutant p53 knockdown to investigate the effect of Pontin on mutant p53-dependent transcriptional regulation.
2015-06-01 | GSE58140 | GEO
Project description:p53 suppresses tumor progression and metastasis by regulating a large set of genes and microRNAs. By profiling 92 primary hepatocellular carcinomas (HCCs) and 9 HCC cell lines, we found that p53 upregulates microRNAs including miR-200 and miR-192 family members. By sequencing TP53 in 92 HCC samples, we classified the 92 samples into two groups (wt and mut). We also classified 9 HCC cell lines by testing p21 expression after DNA-damage mediated p53 activation. We then profiled microRNA expression in 92 HCC tissue samples and 9 HCC celll lines to identify p53-regulated microRNAs.
2011-05-11 | E-GEOD-28661 | biostudies-arrayexpress