In this study we explore the genomic re-wiring of a human colon cancer cell line (LS174T) in which fermentative glycolysis has been fully suppressed by CRISPR/Cas9 to disrupt glucose-6-phosphate isomerase (GPI-KO) or dual disruption of lactate dehydrogenases A and B (LDHAB-DKO). The effects of both KOs, had no effect on loss of viable cell function, corresponding to high concentrations of ATP production vs WT. All three clones were evaluated for transcriptomic changes using GeneChip™ Human Gene 2.1 ST Arrays by Affymetrix Inc assessing for mRNAs and long intergenic non-coding RNA transcripts.
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Sex, Age, Specimen part, Race
View SamplesThis SuperSeries is composed of the SubSeries listed below.
No associated publication
Cell line, Treatment
View SamplesGene expression data from MDA-MB-468 cells grown under variable experimental treatment
No associated publication
Specimen part, Cell line, Treatment
View SamplesSepantronium bromide (YM-155) is believed to trigger apoptosis in tumor cells by inducing a major reduction in baculoviral inhibitor of apoptosis repeat-containing 5 (BIRC 5) also known as survivin. In MDA-MB-231 cells, the toxic effects of YM-155 were equi potent to standard chemotherapy drugs , having an LC50 < 50ng/ml. In this study we investigate whole transcriptome changes occurring at 8 hours of incubation with YM-155, preceding apoptosis as well as at a 20 hour time point. Microarrays were acquired for mRNAs and long intergenic non-coding RNA transcripts using the GeneChip Human Gene 2.1 ST Arrays by Affymetrix Inc.
No associated publication
Specimen part, Cell line
View SamplesThe effects of BSE and 3-OABA on MDA-MB-231 cells were evaluated for effects on the whole transcriptome: including mRNAs and long intergenic non-coding RNA transcripts (lincRNA) using GeneChip Human Gene 2.1 ST Arrays by Affymetrix Inc.
Transcriptomic Profiling of MDA-MB-231 Cells Exposed to <i>Boswellia Serrata</i> and 3-O-Acetyl-B-Boswellic Acid; ER/UPR Mediated Programmed Cell Death.
Specimen part, Cell line, Treatment
View SamplesIn this study, we initially screened over 1400 natural products for capacity to inhibit the kinetic enzyme activity of nuclear HDACs isolated from SK-MEL-3 cells. From these findings we evaluate whole transcriptome changes that occur at a 24 hour time point in SK-ME-3 cells in the presence of a known HDAC inhibitor (Trichostatin A) (1uM) or a natural product HDAC inhibitor Grapeseed Extract (120ug/ml), both tested at sub-lethal concentrations relative to untreated controls. Microarrays were acquired for mRNAs and long intergenic non-coding RNA transcripts using the GeneChip Human 2.1ST ARRAY by Affymetrix Inc
Whole-transcriptomic Profile of SK-MEL-3 Melanoma Cells Treated with the Histone Deacetylase Inhibitor: Trichostatin A.
Cell line, Treatment
View SamplesA common in vitro model for evaluating anti-inflammatory agents is use of lipopolysaccharide (LPS) , a cell wall endotoxic component from gram negative bacteria which evokes a deadly cytokine storm associated with septicemia, septic shock and multi organ failure. In this study , we investigate whole transcriptome changes occurring at 24 hours of incubation with LPS (1ug/ml) in BV2 murine microglia cells. Microarrays were acquired for mRNAs and long intergenic non-coding RNA transcripts using the GeneChip MOGENE 2.1ST ARRAY Arrays by Affymetrix Inc.
No associated publication
Specimen part
View SamplesBackground
Expression quantitative trait loci mapping identifies new genetic models of glutathione S-transferase variation.
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View SamplesBoth the mechanism of action and the factors determining the behavioral response to antidepressants are unknown. It has been shown that antidepressant treatment promotes the proliferation and survival of hippocampal neurons via enhanced serotonergic signaling, but it is still unclear whether hippocampal neurogenesis is responsible for the behavioral response to antidepressants. Furthermore, a large subpopulation of patients fails to respond to antidepressant treatment due to presumed underlying genetic factors. In the present study, we have used the phenotypic and genotypic variability of inbred mouse strains to show that there is a genetic component to both the behavioral and neurogenic effects of chronic fluoxetine treatment, and that this antidepressant induces an increase in hippocampal cell proliferation only in the strains that also show a positive behavioral response to treatment. The behavioral and neurogenic responses are associated with an upregulation of genes known to promote neuronal proliferation and survival. These results suggest that inherent genetic predisposition to increased serotonin-induced neurogenesis is a determinant of antidepressant efficacy.
Genetic regulation of behavioral and neuronal responses to fluoxetine.
Sex, Treatment
View SamplesIn addition to their stem/progenitor properties, mesenchymal stem cells (MSCs) also exhibit various effector functions potent effector (angiogenic, anti-inflammatory, immune-modulatory) functions that are largely paracrine in nature. It is widely believed that effector functions underlie most of the therapeutic potential of MSCs and are independent of their stem/progenitor properties. Here we demonstrate that stem/progenitor and effector functions are coordinately regulated at the cellular level by the transcription factor Twist1 and specified within populations according to a hierarchical model. We further show that manipulation of Twist1 levels by genetic approaches or by exposure to widely used culture supplements including fibroblast growth factor 2 (Ffg2) and interferon gamma (IFN-gamma) alters MSC efficacy in cell-based and in vivo assays in a predictable manner. Thus, by mechanistically linking stem/progenitor and effector functions our studies provide a unifying framework in the form of an MSC hierarchy that models the functional complexity of populations. Using this framework, we developed a Clinical Indications Prediction (CLIP) scale that predicts how donor-to-donor heterogeneity and culture conditions impact the therapeutic efficacy of MSC populations for different disease indications.
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Specimen part
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