Expression profiling by p53 status
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE90 | GEO | 2002/11/25
SECONDARY ACCESSION(S): PRJNA85475
REPOSITORIES: GEO
Similar Datasets
Project description:Human colorectal carcinoma-derived cell lines, p53 -/-, +/-, +/+ at 0 and 12 hrs after growth arrest.
2007-09-28 | E-GEOD-90 | biostudies-arrayexpress
Project description:Human colon carcinoma cells (HCT116) differing in p53 status were exposed to benzo(a)pyrene (BaP) (2.5 and 5 uM for up to 48 h) or anti-benzo(a)pyrene-trans-7,8-dihydrodiol-9,10-epoxide (BPDE)(0.5 and 1 uM for up to 24 h), and their gene expression responses compared by cDNA microarray technology. Keywords: BaP or BPDE exposure
2007-11-13 | GSE9547 | GEO
Project description:Activation of the p53 network plays a central role in the inflammatory stress response associated with ulcerative colitis, and may modulate cancer risk in patients afflicted with this chronic disease. The overall goal of these experiments is to study the gene expression profiles associated with four microenvironmental components of the inflammatory response (NO*, DNA damage, DNA replication arrest, and hypoxia) that result in p53 stabilization and activation. To this end, isogenic HCT116 and HCT116 TP53-/- colon cancer cells were exposed to the NO*-donor Sper/NO, H2O2 (DNA damage), hypoxia, or hydroxyurea (HU, DNA replication arrest), and their mRNA was analyzed using oligonucleotide microarrays. Keywords: time series design
2005-12-01 | GSE3176 | GEO
Project description:P53 inactivation occurs in about 50% of human cancers, where p53-driven p21 activity is devoid and p27 becomes essential for the establishment of the G1/S checkpoint upon DNA damage. Here, we show that the E2F1-responsive lncRNA LIMp27 selectively represses p27 expression and contributes to proliferation, tumorigenicity, and treatment resistance in p53-defective colon adenocarcinoma (COAD) cells. LIMp27 competes with p27 mRNA for binding to cytoplasmically localized hnRNA0, which otherwise stabilizes p27 mRNA leading to cell cycle arrest at the G0/G1 phase. In response to DNA damage, LIMp27 is upregulated in both wild-type and p53-mutant COAD cells, whereas cytoplasmic hnRNPA0 is only increased in p53-mutant COAD cells due to translocation from the nucleus. Moreover, high LIMp27 expression is associated with poor survival of p53-mutant but not wild-type p53 COAD patients. These results uncover a lncRNA mechanism that promotes p53-defective cancer pathogenesis and suggest that LIMp27 may constitute a target for the treatment of such cancers.
| MSV000090292 | MassIVE
Project description:Our previous study revealed that the transcription factor STAT2 promoted the growth of colorectal tumors, but the molecular mechanisms by which STAT2 contributes to tumor promotion are still unknown. Given that alterations in the tumor suppressor p53 gene are very common in colorectal cancer and critical in adenoma-carcinoma transition, we investigated whether STAT2 may also be implicated in disease progression when normal p53 function is disabled. We found Stat2 silencing in colon cancer cells deficient in p53 reduced the capacity of tumor cells to migrate and invade in vitro. We also determined that Stat2 silencing impaired tumor cells to metastasize to the liver. To begin to understand how STAT2 contributes to disease progression, we performed RNA-Seq analysis on colon tumor xenografts with the purpose to identify a STAT2 transcriptome. From this study, we identified a subset of STAT2 regulated genes that in future studies will confirm their role in colon carcinogenesis.
2020-11-17 | GSE137155 | GEO
Project description:Human colon carcinoma cells (HCT116) differing in TP53 status were exposed to aristolochic acid I (AAI) (50 and 100 uM for up to 48 h), and their gene expression responses compared by cDNA microarray technology. Keywords: other
2008-07-28 | GSE10359 | GEO
Project description:A better understanding of how p53 differentially activates cell cycle arrest or cell death is important to maximize benefits of therapeutic strategies dependant by wild-type p53. Here, we report that activation of pro-apoptotic p53 transcriptional targets in colorectal cancer cells imposes a critical, targetable dependence on the long splice form of the caspase-8 regulator FLIP (FLIPL) for survival. Upon Nutlin-3A induced stabilisation p53 directly upregulates FLIPL expression in a manner dependent on Class-I HDAC activity. Preventing FLIPL upregulation with the clinically relevant Class-I selective inhibitor Entinostat promotes apoptosis in response to Nutlin-3A , which predominantly induces growth arrest despite upregulating a range of pro-apoptotic target genes. Cell death in response to Nutlin-3A in FLIPL-depleted cells is mediated through two of p53's canonical transcriptional targets TRAIL-R2 and BAX and is caspase-8-dependent. This work uncovers novel, clinically relevant biology that identifies FLIPL as a key target for overcoming resistance to p53-activating agents.
2020-04-25 | GSE113682 | GEO
Project description:Activation of the p53 network plays a central role in the inflammatory stress response associated with ulcerative colitis, and may modulate cancer risk in patients afflicted with this chronic disease. The overall goal of these experiments is to study the gene expression profiles associated with four microenvironmental components of the inflammatory response (NO*, DNA damage, DNA replication arrest, and hypoxia) that result in p53 stabilization and activation. To this end, isogenic HCT116 and HCT116 TP53-/- colon cancer cells were exposed to the NO*-donor Sper/NO, H2O2 (DNA damage), hypoxia, or hydroxyurea (HU, DNA replication arrest), and their mRNA was analyzed using oligonucleotide microarrays. Cy3-labeled reference probes (untreated) and Cy5-labeled probes (samples exposed for the indicated times) were hybridized to 70-mer oligonucleotide microarrays with 21,329 probes (Qiagen Human Array-Ready Oligo Set, Version 2.0). The arrays were printed by the Advanced Technology Center at the National Cancer Institute. At least two hybridizations (range 2-5) were performed for each sample.
2005-11-30 | E-GEOD-3176 | biostudies-arrayexpress
Project description:Oxaliplatin resistance was induced in 2 colorectal cancer cell lines (LoVo-92, wt-p53 and LoVo-Li, functionally inactive p53) and one ovarian cancer cell line (A2780, wt-p53). Resistance was induced by weekly exposure to oxaliplatin for 4 hrs or 72 hrs with increasing concentrations for a period of 7 months.
2014-03-01 | GSE19992 | GEO
Project description:Oxaliplatin resistance was induced in 2 colorectal cancer cell lines (LoVo-92, wt-p53 and LoVo-Li, functionally inactive p53) and one ovarian cancer cell line (A2780, wt-p53). Resistance was induced by weekly exposure to oxaliplatin for 4 hrs or 72 hrs with increasing concentrations for a period of 7 months
2014-03-01 | GSE20144 | GEO