Cellular plasticity confers cancer cells the ability to adapt to micro-environmental changes, a fundamental requirement for tumour progression and metastasis. The epithelial to mesenchymal transition (EMT) is a transcriptional programme associated with increased cell motility and stemness. Beside EMT, the mesenchymal to amoeboid transition (MAT) has been described during tumour progression but, to date, little is known about its transcriptional control and involvement in stemness. The aim of this study is to investigate (i) the transcriptional profile associated with the MAT programme and (ii) to study whether MAT acquisition in melanoma cancer cells correlate with clonogenic potential to promote tumor growth. Our results demonstrate that MAT programme in melanoma is characterised by increased stemness and clonogenic features of cancer cells, thus sustaining tumour progression. Furthermore, these data suggest that stemness is not an exclusive feature of cells undergoing EMT, but more generally is associated with an increase in cellular plasticity of cancer cells.
Mesenchymal to amoeboid transition is associated with stem-like features of melanoma cells.
Cell line, Treatment
View SamplesEndothelial cells (ECs) express two members of the cadherin family, VE- and N-cadherin. While VE-cadherin induces EC homotypic adhesion, N-cadherin function in ECs remains largely unknown. EC-specific inactivation of either VE- or N-cadherin leads to early foetal lethality suggesting that these cadherins play a non-redundant role in vascular development.
Overlapping and divergent signaling pathways of N-cadherin and VE-cadherin in endothelial cells.
Specimen part, Cell line
View SamplesIn order to identify genes regulated by VE-cadherin expression, we compared a mouse VE-cadherin null cell line (VEC null) with the same line reconstituted with VE-cadherin wild type cDNA (VEC positive). The morphological and functional properties of these cell lines were described previously [Lampugnani,M.G. et al. Contact inhibition of VEGF-induced proliferation requires vascular endothelial cadherin, beta-catenin, and the phosphatase DEP-1/CD148. J. Cell Biol. 161, 793-804 (2003)]. By Affymetrix gene expression analysis we found several genes up-regulated by VE-cadherin, among which claudin-5 reached remarkably high levels. The up-regulation of these genes required not only VE-cadherin expression but also cell confluence suggesting that VE-cadherin clustering at junctions was needed.
Endothelial adherens junctions control tight junctions by VE-cadherin-mediated upregulation of claudin-5.
No sample metadata fields
View SamplesGlobal transcriptome analysis showed that human lymphatic endothelial cells (LECs) grown on a soft matrix exhibit increased GATA2 expression, concomitant with a GATA2-dependent upregulation of genes involved in cell migration and lymphangiogenesis, including the key lymphangiogenic growth factor receptor VEGFR3.
Matrix stiffness controls lymphatic vessel formation through regulation of a GATA2-dependent transcriptional program.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
BMP signaling and cellular dynamics during regeneration of airway epithelium from basal progenitors.
Sex, Specimen part, Treatment
View SamplesThe conducting airway epithelium of the rodent and human lung is made up of about equal proportions of ciliated and secretory cells. In addition, in regions where the epithelium is pseudostratfied, ~30% of the epithelium consists of undifferentiated basal cells (BCs). Evidence suggests that these BCs are multipotent stem cells that can self renew over the long term and give rise to both ciliated and secretory lineages. The goal of this project is to identify cellular and molecular mechanisms by which the basal cells normally maintain the epithelium and repair it after injury.
BMP signaling and cellular dynamics during regeneration of airway epithelium from basal progenitors.
Specimen part, Treatment
View SamplesThe conducting airway epithelium of the rodent and human lung is underlaid by mesenchymal cells that include vasculature, smooth muscle, fibroblasts and cartilage. The goal of this project is to identify cellular and molecular changes in the mesenchyme after injury to the epithelium by exposure to SO2 and which may participate in repair of the epithelium
BMP signaling and cellular dynamics during regeneration of airway epithelium from basal progenitors.
Sex, Specimen part, Treatment
View SamplesTranscription termination factor Rho is essential in enterobacteria. We inhibited Rho activity with bicyclomycin and used microarray experiments to assess Rho function on a genome-wide scale. Rho is a global regulator of gene expression that matches E. coli transcription to translational needs. Remarkably, genes that are most repressed by Rho are prophages and other horizontally-acquired portions of the genome. Elimination of these foreign DNA elements increases resistance to bicyclomycin. Although rho remains essential, such reduced-genome bacteria no longer require Rho cofactors NusA and NusG. Thus, Rho termination, supported by NusA and NusG, is required to suppress the toxic activity of foreign DNA.
Termination factor Rho and its cofactors NusA and NusG silence foreign DNA in E. coli.
Compound
View SamplesTo study the transcriptome of human prostate cancer cells, RNA-seq experiments were performed. Overall design: RNA was harvested after 72h of steroid deprivation to study the basal transcriptome of LNCaP and 22rv1 cells, two human AR-positive prostate cancer cell lines,
Reprogramming of Isocitrate Dehydrogenases Expression and Activity by the Androgen Receptor in Prostate Cancer.
Subject
View SamplesIdentification of TBF1-dependent and SA, elf18-responsive genes in Arabidopsis
The HSF-like transcription factor TBF1 is a major molecular switch for plant growth-to-defense transition.
Specimen part, Treatment
View Samples