ADCY9 encodes AC9, which is 1 of 9 transmembrane AC isoforms (AC1-9) that catalyze the synthesis of cyclic AMP from ATP and are regulated primarily by heterotrimeric G-protein-coupled receptors. We ectopically expressed AC9 in 393P cells and found that, relative to empty vector controls, the AC9 transfectants had higher cyclic AMP levels and were more migratory and invasive in Boyden chambers. We examined the prognostic value of an AC9-regulated gene expression signature derived from 393P_AC9 cells and 393P_vector cells. We probed a compendium of 1,586 clinically annotated human lung adenocarcinomas for the manifestation of the AC9 gene signature and found that the manifestation of the signature was correlated with a significantly shorter duration of survival.
The epithelial-to-mesenchymal transition activator ZEB1 initiates a prometastatic competing endogenous RNA network.
Cell line
View SamplesIn order to discover critical pathways /networks or therapeutic targets in pleural mesothelioma we profiled 55 tumors along with paired normal tissue (for 41 tumors) using Affymetrix U133 plus 2.0 chips
Expression profiling stratifies mesothelioma tumors and signifies deregulation of spindle checkpoint pathway and microtubule network with therapeutic implications.
Specimen part, Disease
View SamplesCharacterization of gene expression changes upon development of taxane-platin drug resistance in NSCLC cells and further, upon treatment of these resistant cells with the Jumonji KDM inhibitor, GSK-J4. Overall design: Comparison of gene expression changes between H1299 Parental cells (chemo-sensitive) and H1299 T18 cells (taxane-platin resistant), and comparison of H1299 T18: GSK-J4 treated vs. H1299 T18: DMSO control.
Taxane-Platin-Resistant Lung Cancers Co-develop Hypersensitivity to JumonjiC Demethylase Inhibitors.
Sex, Age, Treatment, Race, Subject
View SamplesMale and female CD-1 mice were administered dietary Phenobarbital for 2 or 7 days. In-life, enzyme activity, cell proliferation, genomic analysis, and Bench-mark dose modeling was carried out.
Dose-response modeling of early molecular and cellular key events in the CAR-mediated hepatocarcinogenesis pathway.
Specimen part
View SamplesWe examined the transcriptional changes modulated by KDM1A inhibitor NCD-38 by performing global transcriptome analysis. Glioma Stem Cells (GSC10) were treated with either vehicle or NCD-38 for 24 h and the isolated RNA was utilized for RNA-seq analysis. Our results demonstrated that NCD-38 modulated several genes that are involved in unfolded protein response, endoplasmic reticulum stress pathway and NRF-2 mediated oxidative stress response. Overall design: Total RNA was isolated from the GSC10 cells that were treated with vehicle or NCD-38 for 24 hours. Illumina TruSeq RNA Sample Preparation was performed following manufacturer''s protocol. Samples were run on an Illumina HiSeq 2000 in duplicate. The combined raw reads were aligned to UCSC hg19 and genes were annotated by Tophat. Genes were annotated and quantified by HTSeq-DESeq pipeline.
Novel KDM1A inhibitors induce differentiation and apoptosis of glioma stem cells via unfolded protein response pathway.
Treatment, Subject
View SamplesHeme-regulated eIF2 kinase (HRI) is essential for the survival of erythroid precursors in iron and heme deficiency and it also plays a protective role in red blood cell diseases of erythroid protoporphyria and -thalassemia. In this study, we demonstrated for the first time the impairment of GATA-1 and Fog-1 expressions in iron deficiency and the impairment of GATA-1 expression in -thalassemia. Furthermore, HRI is necessary to maintain the GATA-1/Fog-1 induced functions in erythroid differentiation, cell cycle and cell survival by sustaining both expressions of GATA-1 and Fog-1 in iron deficiency and in -thalassemia.
Haem-regulated eIF2alpha kinase is necessary for adaptive gene expression in erythroid precursors under the stress of iron deficiency.
Specimen part
View Samples5 arrays from obese insulin-resistant and lean insulin-sensitive females adipose tissue at fasting and after 3h hyperinsulinemia
Adipose tissue gene expression analysis reveals changes in inflammatory, mitochondrial respiratory and lipid metabolic pathways in obese insulin-resistant subjects.
Sex, Specimen part
View SamplesAnalysis of gene expression profiles of epididymal fat from DIO rats
Assessment of diet-induced obese rats as an obesity model by comparative functional genomics.
No sample metadata fields
View SamplesUnderstanding the biological potential of fetal stem/progenitor cells will help define mechanisms in liver development and homeostasis. We isolated epithelial fetal human liver cells and established phenotype-specific changes in gene expression during continuous culture conditions. Fetal human liver epithelial cells displayed stem cell properties with multilineage gene expression, extensive proliferation and generation of mesenchymal lineage cells, although the initial epithelial phenotype was rapidly supplanted by meso-endodermal phenotype in culture. This meso-endodermal phenotype was genetically regulated through cytokine signaling, including transforming growth factor-b, bone morphogenetic protein, fibroblast growth factors, and other signaling pathways. Reactivation of HNF-3a (FOXA1) transcription factor, a driver of hepatic specification in the primitive endoderm, indicated that the meso-endodermal phenotype represented an earlier developmental stage of cells. We found that fetal liver epithelial cells formed mature hepatocytes in vivo, including after genetic manipulation using lentiviral vectors, offering convenient assays for analysis of further cell differentiation and fate. Taken together, these studies demonstrated plasticity in fetal liver epithelial stem/progenitor cells, offered paradigms for defining mechanisms regulating lineage switching in stem/progenitor cells, and provided potential avenues for regulating cell phenotypes for applications of stem/progenitor cells, such as for cell therapy.
Phenotype reversion in fetal human liver epithelial cells identifies the role of an intermediate meso-endodermal stage before hepatic maturation.
Specimen part
View SamplesWe performed single-cell RNA sequencing (RNA-seq) during the in vitro transition of mouse ESCs (mESCs) from a naïve pluripotent state into epiblast-like cells (EpiLCs), a primed pluripotent state. We derived pseudotime expression trajectories to investigate transcript dynamics of key metabolic regulators, with the aim to identify metabolic pathways that potentially impact on early embryonic cell state transitions. Overall design: Single-cell RNA-seq during the in vitro differentiation of mouse embryonic stem cells (ESCs) in 2i culture conditions (time point t=0h) into epiblast-like cells (EpiLCs) at time points t=24h and t=48h.
Metabolic regulation of pluripotency and germ cell fate through α-ketoglutarate.
Specimen part, Cell line, Subject
View Samples