Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE11673
PROVIDER: PRJNA109157 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The integral role of p53 in tumor suppression has promted many laboratories to perform extensive analyses of signaling pathways downstream of the p53 family of sequence-specific DNA binding transcription factors (p53 and its homologs p63 and p73). Despite the ability of p73 to regulate many p53 family target genes, little is known about the specific pathways that modulate p73 during development, tumorigenesis and tumor therapy. In this study we present a gene signature-based approach for connecting signaling pathways to transcription factors, as exemplified by p73. We generated a p73 gene signature by integrating whole-genome chromatin immunoprecipitation and expression profiling. Experiment Overall Design: H1299 lung carcinoma cells were infected with p73 expressing or control adenovirus for 5 h and then harvested.
2008-10-20 | E-GEOD-11626 | biostudies-arrayexpress
Project description:The integral role of p53 in tumor suppression has promted many laboratories to perform extensive analyses of signaling pathways downstream of the p53 family of sequence-specific DNA binding transcription factors (p53 and its homologs p63 and p73). Despite the ability of p73 to regulate many p53 family target genes, little is known about the specific pathways that modulate p73 during development, tumorigenesis and tumor therapy. In this study we present a gene signature-based approach for connecting signaling pathways to transcription factors, as exemplified by p73. We generated a p73 gene signature by integrating whole-genome chromatin immunoprecipitation and expression profiling. Experiment Overall Design: H1299 lung carcinoma cells were transduced with TAp73beta or GFP expressing adenoviruses. Microarray analysis (on the GFP and TAp73beta samples) and ChIPSeq analysis (on the TAp73beta sample) were performed to identify candidate p73 target genes.
2009-08-30 | E-GEOD-11672 | biostudies-arrayexpress
Project description:Expression data from p73 over-expression in H1299 cells
| PRJNA109151 | ENA
Project description:Transcriptome analysis of methylparaben treated H1299 lung carcinoma cells
| PRJNA560363 | ENA
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:Hepatocyte dedifferentiation is a major source of hepatocellular carcinoma (HCC), but its mechanisms are unknown. We explored the p73 expression in HCC tumors and studied the effects of transcriptionally active p73 (TAp73) in HCC cells. Expression profiles of p73 and patient clinical data were collected from the Genomic Data Commons (GDC) data portal and the TSVdb database, respectively. Global gene expression profiles were determined by pan-genomic 54K microarrays. The Gene Set Enrichment Analysis was used to identify TAp73-regulated gene sets. The effects of TAp73 were analyzed in monolayer cell culture, 3D-tumoroid and xenograft models in zebrafish using western blot, flow cytometry, fluorescence imaging, real-time polymerase chain reaction (RT-PCR), immunohistochemistry and morphological examination. TAp73 was significantly upregulated in HCC, and its high expression indicated poor patient survival. The induced expression of TAp73 caused landscape expression changes including genes involved in growth signaling, cell cycle, stress response, immunity, metabolism and development. HCC cells overexpressing TAp73 had lost hepatocyte lineage biomarkers including ALB, CYP3A4, AFP, HNF4α. In contrast, TAp73 upregulated genes promoting cholangiocyte lineage such as YAP, JAG1 and ZO-1, accompanied with an increase in metastatic ability. Our findings strongly suggest that TAp73 is a major promoter of malignant dedifferentiation of HCC cells Hepatocellular carcinoma (HCC) is a highly complex and heterogeneous type of cancer. Hepatocyte dedifferentiation is one of the important steps in the development of HCC. However, its molecular mechanisms are not well known. In this study, we report that TAp73 which is the major transcriptionally active form of p73 is overexpressed in HCC. Mechanically, TAp73 suppresses the expression of the hepatocyte markers including CYP3A4, AFP, ALB, HNF4a, while increasing the expression of several cholangiocyte markers in HCC cell lines. In conclusion, this report reveals a pro-oncogenic role for TAp73 in liver cancer.
2021-03-10 | GSE162860 | GEO
Project description:Transcriptional profiling of Lung H1299-BRG1 inducible cells
| PRJNA150803 | ENA
Project description:The p53 family is known as a family of transcription factors with functions in tumor suppression and development. Whereas the central DNA binding domain is highly conserved among the three family members p53, p63 and p73, the C-terminal domains (CTDs) are diverse and subject to alternative splicing and post-translational modification. Here we demonstrate that the CTDs strongly influence DNA binding and transcriptional activity. While p53 and the p73 isoform p73ï§ have basic CTDs and form weak sequence-specific protein-DNA complexes, the major p73 isoforms ï¡, ï¢ and ï¤ have neutral CTDs and bind DNA strongly. A basic CTD has been previously shown to enable sliding along the DNA backbone and to facilitate the search for binding sites in the complex genome. Our experiments, however, reveal that a basic CTD also reduces protein-DNA complex stability, intranuclear mobility, promoter occupancy in vivo, transgene activation and induction of cell cycle arrest or apoptosis. A basic CTD in p53 and p73ï§ therefore provides both positive and negative regulatory functions presumably to enable rapid switching of protein activity in response to stress. In contrast, most p73 isoforms exhibit constitutive DNA binding activity consistent with a predominant role in developmental control. Experiment Overall Design: Infection of H1299 cell with different p73/p53 constructs by adenoviral system
2008-10-18 | E-GEOD-8660 | biostudies-arrayexpress
Project description:In our study, we found that profilin 1 (PFN1) promoted non-small cell lung cancer (NSCLC) metastasis.For further investigate the mechanisms of PFN1's roles in NSCLC metastasis, we constructed PFN1 overxpression H1299 cell lines(H1299 PFN1 OE cells). And we sent samples of H1299 PFN1 OE cells and EV cells for TMT based quantative proteome profiling.
2022-04-14 | PXD033148 | Pride
Project description:To examine the effect of metformin on lung cancer biology, human lung H226 and H1299 squamous cell carcinoma cell-lines were grown in RPMI-1640 medium with 10% v/v fetal bovine serum and with or without 15 uM metformin hydrochloride for 7-8 days. Medium (with any metformin) was replaced every two days. Paired cultures with and without metformin were grown and maintained in parallel. Three separate paired cultures, all seeded with same stock of frozen cells, were grown.
2020-02-29 | E-MTAB-8782 | biostudies-arrayexpress