Background: E-cadherin is an adherens junction protein that forms homophilic intercellular contacts in epithelial cells while also interacting with the intracellular cytoskeletal networks. It has roles including establishment and maintenance of cell polarity, differentiation, migration and signalling in cell proliferation pathways. Its downregulation is commonly observed in epithelial tumours and is a hallmark of the epithelial to mesenchymal transition (EMT). Methods: To improve our understanding of how E-cadherin loss contributes to tumorigenicity, we investigated the impact of its elimination from the non-tumorigenic breast cell line MCF10A. We performed cell-based assays and whole genome RNAseq to characterize an isogenic MCF10A cell line that is devoid of CDH1 expression due to an engineered homozygous 4bp deletion in CDH1 exon 11. Results: The E-cadherin-deficient line, MCF10A CDH1-/- showed subtle morphological changes, weaker cell-substrate adhesion, delayed migration, but retained cell-cell contact, contact growth inhibition and anchorage-dependent growth. Within the cytoskeleton, the apical microtubule network in the CDH1-deficient cells lacked the radial pattern of organization present in the MCF10A cells and F-actin formed thicker, more numerous stress fibres in the basal part of the cell. Whole genome RNAseq identified compensatory changes in the genes involved in cell-cell adhesion while genes involved in cell-substrate adhesion, notably ITGA1, COL8A1, COL4A2 and COL12A1, were significantly downregulated. Key EMT markers including CDH2, FN1, VIM and VTN were not upregulated although increased expression of proteolytic matrix metalloprotease and kallikrein genes was observed. Conclusions: Overall, our results demonstrated that E-cadherin loss alone was insufficient to induce an EMT or enhance transforming potential in the non-tumorigenic MCF10A cells but was associated with broad transcriptional changes associated with tissue remodelling. Overall design: Examination of the impact of E-cadherin (CDH1) loss in an isogenic pair of breast cell lines.
E-cadherin loss alters cytoskeletal organization and adhesion in non-malignant breast cells but is insufficient to induce an epithelial-mesenchymal transition.
No sample metadata fields
View SamplesComparison of the meis2b+ and the meis2b- halves of the atrium of the adult zebrafish atrium reveals the existence of two different transcriptional domains. These two domains analogous to that of the two atria in terrestrial vertebrates Overall design: To determine the expression profiles of the Tg(meis2b-reporter)-positive vs -negative atrial compartments, a total of 6 hearts of 3 mpf Tg(meis2b-reporter) zebrafish were micro-dissected. A total of 4 pools were made: the first two pools, each contained 3 Tg(meis2b-reporter)-positive atrial compartments, and the other two contained the Tg(meis2b-reporter)-negative halves.
Distinct myocardial lineages break atrial symmetry during cardiogenesis in zebrafish.
Age, Specimen part, Cell line, Subject
View SamplesTEM differentiated in vitro were exposed to treatments increasing or decreasing their proangiogenic activity. We used microarrays to identify the genes differentially expressed among the treatments and associated to changes in TEM proangiogenic and protumoral functions.
TIE-2 and VEGFR kinase activities drive immunosuppressive function of TIE-2-expressing monocytes in human breast tumors.
Specimen part, Treatment
View SamplesrGal1 (recombinant Galectin-1) vs non treated (Ctrl) pancreatic cancer cell line RWP-1
Targeting galectin-1 inhibits pancreatic cancer progression by modulating tumor-stroma crosstalk.
Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome-wide RNA polymerase II profiles and RNA accumulation reveal kinetics of transcription and associated epigenetic changes during diurnal cycles.
Specimen part
View SamplesCyclic regulatory systems are ubiquitous in cells and tissues. In the liver rhythms in mRNA expression are determined by the homeostatic regulation that operates on daily circumstances. In particular the specific response to nutrients, as well as systemic and peripheral circadian oscillators, contribute to the set up of the hepatic homeostasis at different phases of the day. In this series we used microarrays to detail the global program of gene expression in the mouse liver under physiological daily variations, determined by both the feeding and the circadian cycles.
Genome-wide RNA polymerase II profiles and RNA accumulation reveal kinetics of transcription and associated epigenetic changes during diurnal cycles.
Specimen part
View SamplescAMP receptor protein (CRP, also known as the catabolite activator protein [CAP]) is arguably the best-studied of the global transcription factors of E coli. CRP alone is responsible for regulating at least 283 operons. Upon binding cAMP, the CRP dimer binds DNA and directly interacts with RNA polymerase (RNAP). At Class II promoters, CRP binds near position -41,5 relative to the transcription start site and contacts the amino-terminal domain of the RNAP subunit (RNAP-NTD). This interaction requires AR2, a patch of primarily positively charged residues (H19, H21, E96, and K101) that interact with negatively charged residues on RNAP-NTD. Acetylome analyses consistently detect lysine 100 (K100) of CRP as acetylated. Since K100 is adjacent to the positively charged AR2, we hypothesized that the K100 positive charge may also play a role in CRP function. We further hypothesized that acetylation of K100 would neutralize this positive charge, leading to a potential regulatory mechanism
Influence of Glucose Availability and CRP Acetylation on the Genome-Wide Transcriptional Response of <i>Escherichia coli</i>: Assessment by an Optimized Factorial Microarray Analysis.
No sample metadata fields
View SamplesPMID: 15539473. We compared the gene expression in roots between WT and fit mutant under +Fe and -Fe conditions using ATH1 microarray analysis to explore which genes are affected by the loss of FIT function.
The essential basic helix-loop-helix protein FIT1 is required for the iron deficiency response.
Specimen part, Treatment
View SamplesThe aim of this study was to determine the effect of transgenic Aire expression on the transcriptional profile of a tissue that normally does not express Aire: pancreatic islets. The transcriptional profile of transgenic RIP-Aire27 islets was compared to non-transgenic littermate islets as well as to archival NOD thymic medullary epithelial cells (MEC) data. All data were from non-obese diabetic (NOD) mice
Transcriptional impact of Aire varies with cell type.
No sample metadata fields
View SamplesWe compared the gene expression in roots between WT and uri mutant under +Fe and -Fe conditions using ATH1 microarray analysis to explore which genes are affected by the loss of URI function.
The iron deficiency response in <i>Arabidopsis thaliana</i> requires the phosphorylated transcription factor URI.
Specimen part
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