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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data of NCI-H441 cells stably expressing hsa-mir-365-2 vs empty vector

ABSTRACT: Hsa-mir-365-2 is one of the two precursors that give rise to miR-365. We discovered that miR-365 directly regulates a lung cancer and developmental gene termed thyroid transcription factor 1 (TTF-1 or NKX2-1). Hsa-mir-365-2 was transfected into NCI-H441 cells via retrovirus-mediated gene transfer. Arrays hybridized: Affymetrix GeneChip Human Gene 1.0 ST Array. A total of 4 samples were analyzed. The first two were H441 cells expressing hsa-mir-365-2 and the other two were H441 transfected with empty vector. The class comparison function (significant cutoff, 0.001) of BRB Array Tool (4.1.0 beta_3 release) was used to analyze for differentially expressed genes as a result of enforced expression of hsa-mir-365-2.

ORGANISM(S): Homo sapiens

SUBMITTER: David Mu

PROVIDER: E-GEOD-33672 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data of NCI-H441 cells stably expressing hsa-mir-365-2 vs empty vector

Project description:Hsa-mir-365-2 is one of the two precursors that give rise to miR-365. We discovered that miR-365 directly regulates a lung cancer and developmental gene termed thyroid transcription factor 1 (TTF-1 or NKX2-1). Hsa-mir-365-2 was transfected into NCI-H441 cells via retrovirus-mediated gene transfer. Arrays hybridized: Affymetrix GeneChip Human Gene 1.0 ST Array.

2011-11-15 | GSE33672 | GEO

Homo sapiens

Project description:Expression data of NCI-H441 cells stably expressing hsa-mir-365-2 vs empty vector

| PRJNA148717 | ENA

56afc434-ec9b-4228-9939-fc0a3871593d - samples

Project description:Microglia were derived from iPSCs and treated with mimics and inhibitors of the miRNAs hsa-miR-150-5p, hsa-miR-193a-3p and hsa-miR-19b-3p. RNA-sequencing was then performed to examine the effects of up- and down-regulation of the respective miRNAs.

| EGAD00001006842 | EGA

System-based analyses of brain regions functionally impacted in Parkinson's disease reveals underlying causal mechanisms

Project description:Detailed analysis of disease-affected tissue provides insight into molecular mechanisms contributing to pathogenesis. Substantia nigra, striatum and cortex are functionally connected with increasing degrees of alpha-synuclein pathology in Parkinson's disease. Functional and causal pathway analysis of gene expression and proteomic alterations in these three regions revealed pathways that correlated with deposition of alpha-synuclein. Microarray and RNAseq experiments revealed previously unidentified causal changes related to oligodendrocyte function and synaptic vesicle release and other changes were reflected across all brain regions. Importantly a subset of these changes were replicated in Parkinson's disease blood. Proteomic assessment revealed alterations in mitochondria and vesicular transport proteins that preceded gene gene expression changes indicating defects in translation and/or protein turnover. Our combined approach of proteomics, RNAseq and microarray analyses provides a comprehensive view of the molecular changes that accompany alpha-synculein pathology in Parkinson's disease, and may be instrumental in understanding and diagnosing Parkinson's disease progression. Substantia Nigra (3 normal, 3 PD), Striatum (6 normal, 6 PD), Cortex (5 normal, 5 PD), Cortex non-PD neurodegeneration (2 normal, 3 DLB). Note Sample X201264 was used both for Cortex normal and for Cortex nonPD normal

2014-09-01 | E-GEOD-54282 | biostudies-arrayexpress

A Proneural to Mesenchymal Transition Mediated by NFkB Promotes Radiation Resistance in Glioblastoma (part 1)

Project description:SUMMARY Despite numerous genome-wide association studies involving glioblastoma (GBM), few therapeutic targets have been identified for this disease. Using patient derived glioma sphere cultures (GSCs), we have found that a subset of the proneural (PN) GSCs undergo transition to a mesenchymal (MES) state in a TNFa/NFkB dependent manner with an associated enrichment of CD44 sub-populations and radio-resistant phenotypes. To the contrary, MES GSCs exhibit constitutive NFkB activation, CD44 enrichment and radio-resistance. Patients whose tumors exhibit a higher MES metagene, increased expression of CD44, or activated NFkB were associated with poor radiation response and shorter survival. Our results indicate that NFkB activation mediated MES differentiation and radiation resistance presents an attractive therapeutic target for GBM. SIGNIFICANCE In this study, we show plasticity between the proneural (PN) and mesenchymal (MES) transcriptome signatures observed in glioblastoma (GBM). Specifically, we show that PN glioma sphere cultures (GSCs) can be induced to a MES state with an associated enrichment of CD44 expressing cells and a gain of radio-resistance, which we implicate as NFkB- dependent. Newly diagnosed GBM samples show a direct correlation between radiation response, higher MES metagene, CD44 expression, and NFkB activation. This correlation is also observed in the subset of GBM samples that do not exhibit IDH1 mutation, a favorable prognostic marker. Our results uncover a previously unknown link between subtype plasticity that is regulated by NFkB. Inhibition of NFkB activation can directly impact radio-resistance and presents an attractive therapeutic target for GBM. Gene expression data for 17 isolated Glioma Stem Cells

2013-08-15 | E-GEOD-49161 | biostudies-arrayexpress

miRNA expression data from MCF-7 cells, overexpressing ANXA1

Project description:Annexin 1 (ANXA1), an endogenous anti-inflammatory protein which modulates cellular processes such as proliferation, differentiation and apoptosis has been implicated in cancer initiation and progression. ANXA1 was previously shown to be regulated by hsa-miR-196a and promoted cell proliferation and anchorarge-dependent growth and suppressed apoptosis. However, whether ANXA1 itself regulates miRNA expression is unknown. Therefore, in this study, we investigated the regulation of miRNA by ANXA1 in breast cancer cells. Using microarray technology, 12 miRNAs were found to be significantly and consistently downregulated in MCF-7 cells (MCF-V5) overexpressing ANXA1 overexpressing MCF-7 cells (MCF-V5). Hsa-miR-26b* and hsa-miR-562 were chosen for further investigation.The data suggest that miR-26b* and miR-562 may play a role in ANXA1-induced migration and possibly angiogenesis by targeting NFKB and point towards a potential therapeutic target for breast cancer. Breast cancer MCF-7 cells (MCF-V5) overexpressing ANXA1 were cultured for RNA extraction and hybridization on Affymetrix miRNA microarrays. These were compared against the control, which were MCF-7 cells (MCF-EV) carrying an empty expression vector. Expression analyses were carried out in triplicates

2015-01-05 | E-GEOD-54439 | biostudies-arrayexpress

A Proneural to Mesenchymal Transition Mediated by NFkB Promotes Radiation Resistance in Glioblastoma (part 2)

2013-08-15 | E-GEOD-49162 | biostudies-arrayexpress

A Proneural to Mesenchymal Transition Mediated by NFkB Promotes Radiation Resistance in Glioblastoma

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-08-15 | E-GEOD-49009 | biostudies-arrayexpress

5b763f6e-2031-4d46-913d-ee7491e7e50c - samples

Project description:iPSC-derived neurons were treated with mimics and inhibitors of the miRNAs miR-150-5p, hsa-mir-193a-3p and hsa-miR-19b-3p. RNA-sequencing was then performed to examine the effects of miRNA up-regulation and inhibition.

| EGAD00001006844 | EGA

Genome-wide analysis of gene expression in human iPSCs and NSCs engineered by safe-harbor TALEN-mediated gene targeting

Project description:Human iPSCs and NSCs were engineered by AAVS1 and/or C13 safe-harbor TALENs which mediated targeted integration of various reporter genes at single or dual safe-harbor loci. Multiple clones of targeted human iPSCs were used to compare with parental untargeted NCRM5 iPSCs. Polyclonal targeted human NSCs were used to compare with their parental untargeted NCRM1NSCs or H9NSCs. Total RNA obtained from targeted human iPSCs or NSCs compared to untargeted control iPSCs or NSCs.

2014-09-01 | E-GEOD-55975 | biostudies-arrayexpress

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