Homo sapiens
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ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-18182
PROVIDER: PRJNA174034 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression profile of lung adenocarcinoma, A549 cells following induction of non metastatic 2 (NME2/NM23 H2)
| PRJNA173068 | ENA
Project description:Genome-wide maps of NME2 in A549 lung adenocarcinoma cells.
| PRJNA173992 | ENA
Project description:Expression profile of lung adenocarcinoma, A549 cells following targeted depletion of non metastatic 2 (NME2/NM23 H2)
2025-01-24 | E-GEOD-18182 | ExpressionAtlas
Project description:Transcription profiling of human adipose derived stem cells before induction and at two time points after induction of differentiation
2025-01-22 | E-MEXP-1216 | ExpressionAtlas
Project description:This SuperSeries is composed of the following subset Series: GSE18182: Expression profile of lung adenocarcinoma, A549 cells following targeted depletion of non metastatic 2 (NME2/NM23 H2) GSE18284: Genomic binding sites of non-metastatic 2 (NME2) across promoters in lung cancer A549 cells Refer to individual Series
2011-02-08 | E-GEOD-18285 | biostudies-arrayexpress
Project description:It is widely believed that reorganization of nucleosomes result in availability of binding sites that engage transcription factors during eukaryotic gene regulation. Recent findings, on the other hand, suggest that transcription factors induced as a result of physiological perturbations directly (or in association with chromatin modifiers) may alter nucleosome occupancy to facilitate DNA binding. Although, together these suggest a close relationship between transcription factor binding and nucleosome reorganization, the nature of the inter-dependency, or to what extent it influences regulatory transcription is not clear. Moreover, since most studies used physiolgical pertubations that induced multiple transcription factor chromatin modifiers, the relatively local (or direct) effect of transcription factor binding on nucleosome occupancy remains unclear. With these in mind, we used a single transcription factor to induce physiological changes, representing metastatic (aggressive cancer) and the corresponding non-metastatic state, in human cancer cells. Following characterization of the two states (before and after induction of the transcription factor) we determined: (a) genome wide binding sites of the transcription factor, (b) promoter nucleosome occupancy and (c) transcriptome profiles, independently in both conditions. Interestingly, we find only ~20% of TF binding results from nucleosome reorganization - however, almost all corresponding genes were transcriptionally altered. Whereas, in cases where TF-occupancy was independent of nucleosome repositioning (in close vicinity), or co-occurred with nucleosomes, only a small fraction of the corresponding genes were expressed/repressed. Together, these indicate a model where TF occupancy only when coupled with nucleosome repositioning in close proximity is transcriptionally active. This, to our knowledge, for the first time also helps explain why genome wide TF occupancy (e.g., from ChIP-seq) is typically associated with only a small fraction of genes that change expression. For expression profiling of cells in NME2-induced conditions, A549 cells were transfected with pcDNA-NME2-MYC or pcDNA-MYC (control). RNA was isolated from the cells 48h after transfection using the trizol method (Sigma) as per manufacturerM-bM-^@M-^Ys protocol. Total RNA was processed to hybridize to Illumina Human HT-12 v4 Expression BeadChip as per manufacturerM-bM-^@M-^Ys instructions. Three biological replicates were averaged and data was analyzed using BeadStudio (P <0.05 of fold change).
2014-08-04 | E-GEOD-40194 | biostudies-arrayexpress
Project description:Non-metastatic 2 (NME2) is an established metastases suppressor in multiple human cancer types. However, the molecular mechanisms of NME2 action remain insufficiently resolved. We recently validated the transcription regulatory activity of NME2 with respect to control of proto-oncogene c-MYC expression. We hypothesized that large scale transcriptional potential of NME2 may be at the core of metastases suppression by NME2. Using a combination of high throughput genomic assays such as chromatin immunoprecipitation coupled to promoter array hybridization (ChIP-chip) and gene expression profiling, we characterized the transcriptional roles of NME2. Specifically, we found a set of NME2 target genes which changed expression upon selective depletion of NME2 in a lung cancer cell line, A549. The analysis of gene expression suggested control of various biological pathways esp. cell adhesion and apoptosis by NME2 target genes which could be important in regulation of metastases. For transcriptome analysis, total RNA was purified from A549 cells transiently silenced for NME2 (siRNA duplex against NME2/ NM23 H2(Santa Cruz)) or transfected with control siRNA duplexes. Isolated RNA was converted to cDNA, transcribed in vitro to synthesize biotinylated cRNA, and hybridized to Affymetrix HG-U133 plus 2.0 GeneChip oligonucleotide microarrays, according to manufacturer’s instructions. Three biological replicates were averaged and significance analysis performed using GCOS (P <0.005 of fold change).
2011-02-08 | E-GEOD-18182 | biostudies-arrayexpress
Project description:Genomic binding sites of non-metastatic 2 (NME2) across promoters in lung cancer A549 cells
| PRJNA123513 | ENA