Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-18182
PROVIDER: PRJNA173068 | ENA |
REPOSITORIES: ENA
Similar Datasets
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:Expression profile of lung adenocarcinoma, A549 cells following targeted depletion of non metastatic 2 (NME2/NM23 H2)
2015-08-07 | E-GEOD-18182 | ExpressionAtlas
Project description:Expression profile of lung adenocarcinoma, A549 cells following targeted depletion of non metastatic 2 (NME2/NM23 H2)
| PRJNA123489 | ENA
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:Non-metastatic 2 (NME2) is one of the first discovered suppressors of metastases. However, the molecular mechanisms underlying its anti-metatsic activity remain insufficiently characterized. We hypothesized that large scale transcriptional potential of NME2 might be at the core of this function. Using a combination of gene expression meta-analysis, and high throughput genomic assays, we explored the transcriptional targets of NME2. Specifically, we found >250 binding sites of NME2 across human gene promoters. Several of the novel targets identified in this way regulated cell adhesion and survival. We subsequently constructed NME2 target gene network which delineated a transcriptional program responsive to NME2 capable of restricting metastasis. Three sets of ChIP vs. mock-ChIP experiments were done. pcDNA plasmid was transfected to lung cancer, A549 cells to express NME2 tagged with MYC epitope which was subsequently immunoprecipitated using anti-MYC antibodies (after 48 hours of transfection). Non-specific IgG was used for mock immunoprecipitation.
2011-02-08 | E-GEOD-18284 | 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.
2011-02-08 | GSE18182 | GEO
Project description:Genome-wide maps of NME2 in A549 lung adenocarcinoma cells.
| PRJNA173992 | ENA
Project description:Genomic binding sites of non-metastatic 2 (NME2) across promoters in lung cancer A549 cells
| PRJNA123513 | ENA
Project description:To determine the signaling networks that are dysregulated in cisplatin-resistant non-small cell lung cancer, noncoding RNA expression data were obtained from, and compared between, the lung adenocarcinoma cell line, A549, and its cisplatin-resistant derivative, A549/CDDP. Noncoding RNA expression data from a cisplatin-sensitive lung adenocarcinoma cancer cell line (A549) were collected and compared to noncoding RNA expression data from a cisplatin-resistant cell line (A549/CDDP). 3 independent experiments were completed for both the sensitive and resistant cell lines.
2013-01-15 | E-GEOD-43249 | biostudies-arrayexpress