Mastic oil from Pistacia lentiscus variation chia, a blend of bioactive terpenes with recognized medicinal properties, has been recently shown to exert anti-tumor activity. Lewis lung carcinoma (LLC) cells are mastic oil-susceptible cells and were used in this work to study the effects of mastic oil at the transcriptomic level.
A transcriptomic computational analysis of mastic oil-treated Lewis lung carcinomas reveals molecular mechanisms targeting tumor cell growth and survival.
Cell line
View SamplesAssessment of the putative differential gene expression profiles in high osmolality-treated bovine nucleus pulposus intervertebral disc cells for a short (5 h) and a long (24 h) time period. Identification of novel genes up- or down-regulated as an early or a late response to hyperosmotic stress.
Deficiency in the α1 subunit of Na+/K+-ATPase enhances the anti-proliferative effect of high osmolality in nucleus pulposus intervertebral disc cells.
Specimen part
View SamplesHuman Umbilical Vein Endothelial Cells were treated with three newly synthesized compounds and DMSO as vehicle. Total RNA was isolated 6 and 24h after treatment and gene expression analysis was performed. Three independent experiments were performed, corresponding to rep1, rep2 and rep3. Experiment 1 (rep1) contained all substances at both time points tested. Experiment 2 (rep2) contained two of the compounds and control DMSO at both time points. Experiment 3 (rep3) contained the third compound and control DMSO at both time points.
Novel pyrazolopyridine derivatives as potential angiogenesis inhibitors: Synthesis, biological evaluation and transcriptome-based mechanistic analysis.
Specimen part, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Radiogenomic Analysis of F-18-Fluorodeoxyglucose Positron Emission Tomography and Gene Expression Data Elucidates the Epidemiological Complexity of Colorectal Cancer Landscape.
Specimen part
View SamplesColorectal cancer is a highly heterogeneous disease, with variable molecular pathogenesis, involving multiple genomic and epigenetic alterations. Despite the significant advances in the diagnosis and treatment of colorectal cancer, it remains a major cause of morbidity and mortality, especially for countries in Northern America and Europe, as also in New Zealand & Australia. In this direction, the introduction of gene expression signatures derived from multiple layers of molecular & clinical dissection, may resolve the problems of heterogeneity and improve robust disease stratification
Radiogenomic Analysis of F-18-Fluorodeoxyglucose Positron Emission Tomography and Gene Expression Data Elucidates the Epidemiological Complexity of Colorectal Cancer Landscape.
Specimen part
View SamplesColorectal cancer is a highly heterogeneous disease, with variable molecular pathogenesis, involving multiple genomic and epigenetic alterations. Despite the significant advances in the diagnosis and treatment of colorectal cancer, it remains a major cause of morbidity and mortality, especially for countries in Northern America and Europe, as also in New Zealand & Australia. In this direction, the introduction of gene expression signatures derived from multiple layers of molecular & clinical dissection, may resolve the problems of heterogeneity and improve robust disease stratification.
Radiogenomic Analysis of F-18-Fluorodeoxyglucose Positron Emission Tomography and Gene Expression Data Elucidates the Epidemiological Complexity of Colorectal Cancer Landscape.
Specimen part
View SamplesRNA editing is a mutational mechanism that specifically alters the nucleotide content in sets of transcripts while leaving their cognate genomic blueprint intact. Editing has been detected from bulk RNA-seq data in thousands of distinct transcripts, but apparent editing rates can vary widely (from under 1% to almost 100%). These observed editing rates could result from approximately equal rates of editing within each individual cell in the bulk sample, or alternatively, editing estimates from a population of cells could reflect an average of distinct, biologically significant editing signatures that vary substantially between individual cells in the population. To distinguish between these two possibilities we have constructed a hierarchical Bayesian model which quantifies the variance of editing rates at specific sites using RNA-seq data from both single cells and a cognate bulk sample consisting of ~ 106 cells. The model was applied to data from murine bone-marrow derived macrophages and dendritic cells, and predicted high variance for specific edited sites in both cell types tested. We then 1 validated these predictions using targeted amplification of specific editable transcripts from individual macrophages. Our data demonstrate substantial variance in editing signatures between single cells, supporting the notion that RNA editing generates diversity within cellular populations. Such editing-mediated RNA-level sequence diversity could contribute to the functional heterogeneity apparent in cells of the innate immune system. Overall design: 26 samples were subjected to RNA-seq: 24 single WT macrophages, and 2 bulk samples (Apobec1 WT and KO macrophages), consisting of 500,000-1 million cells each.
RNA editing generates cellular subsets with diverse sequence within populations.
Specimen part, Cell line, Subject
View SamplesThe metabolic syndrome (MetS) is characterized by the presence of metabolic abnormalities that include abdominal obesity, dyslipidemia, hypertension, increased blood glucose/insulin resistance, hypertriglyceridemia and increased risk for cardiovascular disease (CVD). The ApoE*3Leiden.human Cholesteryl Ester Transfer Protein (ApoE3L.CETP) mouse model manifests several features of the MetS upon high fat diet (HFD) feeding. Moreover, the physiological changes in the white adipose tissue (WAT) contribute to MetS comorbidities. The aim of this study was to identify transcriptomic signatures in the gonadal WAT of ApoE3L.CETP mice in discrete stages of diet-induced MetS.
Transcriptome analysis of the adipose tissue in a mouse model of metabolic syndrome identifies gene signatures related to disease pathogenesis.
Sex, Age, Specimen part
View SamplesMediator is regarded a general co-activator of RNA-Polymerase II dependent transcription but not much is known about its function and regulation in mouse pluripotent embryonic stem cells (mESC). One means of controlling Mediator function is provided by binding of the Cdk8 module (Med12, Cdk8, Ccnc and Med13) to Mediator. Here we report that the Cdk8 module subunit Med12 operates together with PRC1 to silence developmental key genes in the pluripotent state. At the molecular level, PRC1 is required to assemble ncRNA containing Med12-Mediator complexes at promoters of repressed genes. In the course of cellular differentiation the H2A-ubiquitin binding protein Zrf1 abrogates PRC1-Med12 binding and facilitates the recruitment of Cdk8 into Mediator. Remodeling of the Mediator-associated protein complex converts Mediator into a transcriptional enhancer that mediates ncRNA-dependent activation of Polycomb target genes Overall design: RNAseq of pluripotent (control, shNMC, shRing1b, shMed12, shCdk8, shZrf1) and early differentiating (control, shNMC, shMed12, shCdk8, shZrf1) stem cells in triplicates. Control would be normal E14TG2A mESCs. shNMC refers to E14TG2A cells stably transfected with a short hairpin that has no mammalian targets (Non Mammalian Control). All the other samples are indeed stably transfected with short hairpins against the indicated genes.
Dual role of Med12 in PRC1-dependent gene repression and ncRNA-mediated transcriptional activation.
Specimen part, Cell line, Subject
View SamplesGlioblastoma multiforme is the most lethal form of glioma with an overall survival at 5 years nearly null, which mainly results from acquired resistance to therapies. Large scale sequencing studies on human cancer biopsies defined IRE1alpha as the fifth most oncogenic mutated kinase in human cancer. IRE1alpha is a major component of the Unfolded Protein Response signaling and increasing evidence suggests that it is a central player in GBM development.
Dual IRE1 RNase functions dictate glioblastoma development.
Specimen part, Cell line
View Samples