E-GEOD-35972
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA151623
PROVIDER: E-GEOD-35972 | ExpressionAtlas | 2025-01-24
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-35972-analysis-methods.tsv | Tabular | |||
| E-GEOD-35972-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-35972-configuration.xml | Xml | |||
| E-GEOD-35972-percentile-ranks.tsv | Tabular | |||
| E-GEOD-35972.condensed-sdrf.tsv | Tabular |
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Similar Datasets
Project description:Class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of p53 mutants in pancreatic cancer cells. Our data reveal that the inhibition of these HDACs with HDAC inhibitors (such as Entinostat) as well as the specific genetic elimination of HDAC1 and HDAC2 leads to a reduced expression of p53 mRNA levels and a subsequent depletion of mutant p53 protein expression. To investigate other tumor entities we also tested the human colon carcinoma cell line HCT-116, which was treated for 24h with 2µM Entinostat or treated with vehicle control. Total mRNA was isolated and checked for integrity. According to manufacture's recommendation the samples were subjected to microarray analysis using the Affymetrix Human Gene ST 2.0 array chip to discover differentially expressed genes.
2016-06-09 | E-MTAB-4303 | biostudies-arrayexpress
Project description:In most lymphomas, p53 signaling pathway is inactivated by various mechanisms independent to p53 gene mutations or deletions. In many cases, p53 function is largely regulated by alterations in the protein abundance levels by the action of E3 ubiquitin-protein ligase MDM2, targeting p53 to proteasome-mediated degradation. In the present study, an integrating transcriptomics and pro-teomics analysis was employed to investigate the effect of p53 activation by a small-molecule MDM2-antagonist, nutlin 3a, on three lymphoma cell models following p53 activation. Our analy-sis revealed a system-wide nutlin 3a-associated effect in all examined lymphoma types, identifying in total of 4037 differentially affected proteins involved in a plethora of pathways, with significant heterogeneity among lymphomas. Our findings include known p53-targets and novel p53 activa-tion effects, involving transcription, translation, or degradation of protein components of path-ways, such as a decrease in key members of PI3K/mTOR pathway, heat-shock response, and gly-colysis, and an increase in key members of oxidative phoshosphorylation, autophagy and mito-chondrial translation. Combined inhibition of HSP90 or PI3K/mTOR pathway with nutlin 3a-mediated p53-activation enhanced the apoptotic effects suggesting a promising strategy against human lymphomas. Integrated omic profiling after p53 activation offered novel insights on the regulatory role specific proteins and pathways may have in lymphomagenesis.
2023-07-30 | PXD009290 | Pride
Project description:Primary objectives: The primary objective of the study is to assess whether the administration of p53-SLP together with the local application of imiquimod or the injection of interferon-alfa is safe and able to induce an immune response specific to p53.
Primary endpoints: Safety will be assessed during the whole study by collecting all adverse events (with a focus on administration site reactions), vital signs, blood-chemistry and haematological parameters. Immunogenicity will be assessed by an array of complementary immunological assays which focus on p53-specific T-cell proliferation, enumeration of circulating IFNγ-producing T-cells, Th1/Th2 cytokine production, and p53 protein recognition by circulating and vaccine-site-homing T-cells.
| 2524913 | ecrin-mdr-crc
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:Abstract: Epithelial ovarian carcinomas (OC) are particularly deadly due to intratumoral heterogeneity, resistance to standard-of-care therapies, and poor response to alternative treatments such as immunotherapy. Targeting the OC epigenome with DNA methyltransferase inhibitors (DNMTi) or histone deacetylase inhibitors (HDACi) increases immune signaling and recruits CD8+ T cells and NK cells to fight OC in murine models. This increased immune activity is caused by increased transcription of repetitive elements (RE) that form double-stranded RNA (dsRNA) and trigger an interferon response. To understand which REs are affected by epigenetic therapies in OC, we assessed the effect of DNMTi and HDACi on OC cell lines and patient samples. Subfamily-level (TEtranscripts) and individual locus-level (Telescope) analysis of REs showed that DNMTi treatment upregulated more REs than HDACi treatment. Upregulated REs were predominantly LTR and SINE subfamilies, and SINEs exhibited the greatest loss of DNA methylation upon DNMTi treatment. Cell lines with TP53 mutations exhibited significantly fewer upregulated REs with epigenetic therapy than wild type TP53 cell lines. This observation was validated using isogenic cell lines; the TP53 mutant cell line had significantly higher baseline expression of REs but upregulated fewer upon epigenetic treatment. In addition, p53 activation increased expression of REs in wild type but not mutant cell lines. These data give a comprehensive, genome-wide picture of RE chromatin and transcription-related changes in OC after epigenetic treatment and implicate p53 in RE transcriptional regulation. The data in this data series represent the analysis of P53 ChIPseq libraries generated from the A2780 ovarian carcinoma cell lines. Each cell line was treated with Nutlin-3A or 5-azacytidine. Each library was sequenced, trimmed, aligned, and analyzed with MACS2 and IDR. The ChIP-seq peaks were used to analyze how P53 regulated repetitive element transcription in response to epigenetic therapies.
2021-08-17 | GSE182114 | GEO
Project description:In colorectal cancer, p53 is commonly inactivated, associated with chemo-resistance, and marks the transition from non-invasive to invasive disease. Cancers, including colorectal cancer, are thought to be diseases of aberrant stem cell populations, as stem cells are able to self-renew, making them long-lived enough to acquire mutations necessary to manifest the disease. We have shown that extracts from sweet sorghum stalk components eliminate colon cancer stem cells (CCSC) in a partial p53-dependent fashion. However, the underlying mechanisms are unknown. In the present study, CCSC were transfected with short hairpin-RNA against p53 (CCSC p53 shRNA) and treated with sweet sorghum phenolics extracted from different plant components (dermal layer, leaf, seed head and whole plant). While all components demonstrated anti-proliferative and pro-apoptotic effects in CCSC, phenolics extracted from the dermal layer and seed head were more potent in eliminating CCSC by elevating caspases 3/7 activity, PARP cleavage, and DNA fragmentation in a p53-dependent and p53-independent fashion, respectively. Further investigations revealed that the anti-proliferative and pro-apoptotic effects were associated with decreases in beta-catenin protein levels, and beta-catenin targets cyclin D1, cMyc, and survivin. These results suggest that the anti-proliferative and pro-apoptotic effects of sweet sorghum extracts against human colon cancer stem cells are via suppression of Wnt/beta-catenin pro-survival signaling in a p53-dependent (dermal layer) and partial p53-independent (seed head) fashion. LCMS used to identify phenolic compounds associated with extract activity
2014-05-01 | MTBLS69 | MetaboLights
Project description:To globally evaluate to what extend type-1 p53 mutant transcription activity can be restored by arsenic trioxide (ATO) (compared to wild-type p53), p53-null U937 cells introduced with 10 frequent type-1 p53, type-3 p53-R273H (negative control), empty vector or wild-type p53 were treated with or without 1 μg/mL ATO. mRNA was isolated and then subject to deep sequencing, using Illumina HiSeq. The sequence reads that passed quality filters were analyzed using Cutadapt. Results and conclusions: The type-1 p53 mutants are the major cellular targets of ATO in the current cell contexts. The expression profiles of well-established p53 targets in cells expressing wild-type p53 highly correlated with the ones in cells expressing ATO-rescued type-1 mutants, but not those in cells expressing ATO-treated R273H. In cells harboring type-1 mutants, the median expression levels of these targets were elevated by ATO to extents comparable to wild-type p53.
2024-08-01 | GSE182565 | GEO
Project description:The effects of demycarosyl-3D-M-NM-2-D-digitoxosyl-mithramycin SK (DIG-MSK; EC-8042), a novel analogue of the antitumor antibiotic mithramycin A, on gene transcription were examined in human A2780 ovarian carcinoma cells. DIG-MSK down-regulated a different set of genes depending on the drug concentration. Moreover, several genes were significantly up-regulated. These results are rationalized in terms of DIG-MSK competition with Sp1 transcription factor for binding to consensus C/G-rich tracts encompassed in gene promoters. Human A2780 ovarian carcinoma cells were treated with either 8 nM or 80 nM DIG-MSK for 24 h, and RNA was extracted from treated cells as well as from untreated (control) cells.
2014-08-13 | E-GEOD-46926 | biostudies-arrayexpress
Project description:We performed p53 ChIP-seq analysis of Nutlin-treated HCT116 cells to identify high-confident p53 regulated targets. And we performed ChIP-seq using an anti-p53 antibody in HCT116 cells treated with control or iASPP RNAi to identify iASPP regulated p53 targets.
2019-09-23 | GSE113338 | GEO
Project description:Ovarian cancer is a deadly gynecological malignancy for which novel biomarkers and therapeutic targets are imperative for improving survival. To investigate the role of histone H1 in ovarian cancer cells, we overexpress a histone H1 variant, H1.3, in the OVCAR-3 epithelial ovarian cancer cell line. RNA was extracted from OV-3/H1.3(H) cells (OVCAR-3 with overexpression of H1.3) and control cells of OVCAR-3 transfected with vectors without H1.3. The microarray chip used was human Affymetrix ST1.0 array. Gene expression changes caused by overexpression of H1.3 in OVCAR-3 cells were identified.
2014-10-31 | GSE61692 | GEO