To elucidate the mechanisms by which Nrf2 regulates cell growth, we performed global gene expression profiling of A549 lung cancer cells with knockdown of Nrf2. Gene networks associated with carbohydrate metabolism and drug metabolism were significantly downregulated in Nrf2-depleted A549 cells. Gene Set Enrichment Analysis revealed significant enrichment of genes associated with carbohydrate catabolic processes, positive regulation of metabolic processes, PPP, and arachidonic acid metabolism. In summary, this analysis revealed that Nrf2 positively regulates transcription of genes that play key roles in central carbon metabolism.
Transcription factor NRF2 regulates miR-1 and miR-206 to drive tumorigenesis.
Specimen part, Cell line
View SamplesWe examine the potential of Kras as a metabolic target in lung cancer using the KrasLSL-G12D lung cancer model. We demonstrate that mutant Kras drives a lipogenic gene expression program, and that fatty acid synthesis is important in Kras-induced tumorigenesis.
De novo lipogenesis represents a therapeutic target in mutant Kras non-small cell lung cancer.
Specimen part
View SamplesMost cell culture experiments utilize media containing fetal calf serum. Results are often interpreted regarding importance to human pathways. We studied gene expression in mouse macrophages grown in the absence of serum, and in fetal calf serum, mouse serum, and human serum using genome wide expression systems in resting conditions and after stimulation with lipopolysaccharide.
No associated publication
Specimen part, Treatment
View SamplesAffymetrix MG430 2.0 expression levels of wild-type (STHdhQ7/Q7), 3NP-treated wild-type (STHdhQ7/Q7+3-NP), and mutant (STHdhQ111/Q111) striatal cells
Unbiased gene expression analysis implicates the huntingtin polyglutamine tract in extra-mitochondrial energy metabolism.
No sample metadata fields
View SamplesAnalysis of gene expression data in two C.elegans mutant strains: KP3293 tom-1(nu468) and KP3365 unc-43(n1186); hif-1(nu469). These results support the utility of microarray hybridizations to facilitate positional cloning.
Using microarrays to facilitate positional cloning: identification of tomosyn as an inhibitor of neurosecretion.
No sample metadata fields
View SamplesNA
No associated publication
Sex, Age, Specimen part, Cell line
View SamplesSingle-cell RNA-seq reveals dynamic estrogen-stimulated metabolic reprogramming in breast cancer cell lines
No associated publication
Sex, Specimen part, Cell line
View SamplesSingle-cell RNA-seq reveals dynamic estrogen-stimulated metabolic reprogramming in breast cancer cell lines
No associated publication
Sex, Age, Specimen part, Cell line
View SamplesBackground & Aims: Genome-wide gene expression (GWGE) profiles of mucosal colonic biopsies have suggested the existence of a continuous inflammatory state in quiescent ulcerative colitis (UC). The aim of this study was to use DNA microarray-based GWGE profiling of mucosal colonic biopsies and isolated colonocytes from UC patients and controls in order to identify the cell types responsible for the continuous inflammatory state. Methods: Adjacent mucosal colonic biopsies were obtained endoscopically from the descending colon in patients with active UC (n=8), quiescent UC (n=9), and with irritable bowel syndrome (controls, n=10). After isolation of colonocytes and subsequent extraction of total RNA, GWGE data were acquired using Human Genome U133 Plus 2.0 GeneChip Array (Affymetrix, Santa Clara, CA). Data analysis was carried out by principal component analysis and projection to latent structure-discriminant analysis using the SIMCA-P11 software (Umetrics, Ume, Sweden). Results: A clear separation between active UC, quiescent UC and control biopsies were found, whereas the model for the colonocytes was unable to distinguish between quiescent UC and controls. The differentiation between quiescent UC and control biopsies was governed by unique profiles containing gene expressions with significant fold changes. These primarily belonged to the family of homeostatic chemokines revealing a plausible explanation to the abnormal regulated innate immune response seen in patients with UC. Conclusion: This study has demonstrated the presence of a continuous inflammatory state in quiescent UC, which seems to reflect an altered gene expression profile of lamina propria cells.
Genome-wide gene expression analysis of mucosal colonic biopsies and isolated colonocytes suggests a continuous inflammatory state in the lamina propria of patients with quiescent ulcerative colitis.
No sample metadata fields
View SamplesNA
No associated publication
Sex, Age, Specimen part, Cell line
View Samples