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Comparison of the RNA expression profile between P-cadherin over-expressing BLM melanoma cells and empty-vector control cells

ABSTRACT: Van Marck et al. (Cancer Research, 2005) published that overexpression of P-cadherin in a melanoma cell line promoted homo- and heterotypic cell-cell adhesion, induced an epitheloïd morphology, and impaired cancer cell invasion. Therefore, we wanted to compare the RNA expression profile between the empty vector control cells and the P-cadherin overexpression variant. This experiment could provide us with effector molecules of P-cadherin that mediate its anti-invasive function.

ORGANISM(S): Homo sapiens

PROVIDER: GSE23360 | GEO | 2011/06/01

SECONDARY ACCESSION(S): PRJNA131453

REPOSITORIES: GEO

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Comparison of the RNA expression profile between P-cadherin over-expressing BLM melanoma cells and empty-vector control cells

Project description:Van Marck et al. (Cancer Research, 2005) published that overexpression of P-cadherin in a melanoma cell line promoted homo- and heterotypic cell-cell adhesion, induced an epitheloïd morphology, and impaired cancer cell invasion. Therefore, we wanted to compare the RNA expression profile between the empty vector control cells and the P-cadherin overexpression variant. This experiment could provide us with effector molecules of P-cadherin that mediate its anti-invasive function. 2 samples were analyzed, each with 2 replicates

2011-06-01 | E-GEOD-23360 | biostudies-arrayexpress

Comparison of the RNA expression profile between P-cadherin over-expressing BLM melanoma cells and empty-vector control cells

| S-ECPF-GEOD-23360 | biostudies-other

Effects of cadherin mediated contact normalization on oncogenic Src kinase mediated gene expression and protein phosphorylation

Project description:Nontransformed cells form heterotypic cadherin junctions with adjacent transformed cells to inhibit tumor cell growth and motility. Transformed cells must override this form of growth control, called contact normalization, to invade and metastasize during cancer progression. Heterocellular cadherin junctions between transformed and nontransformed cells are needed for this process. However, specific mechanisms downstream of cadherin signaling have not been clearly elucidated. Here, we utilized a b-catenin reporter construct to determine if contact normalization affects Wnt signaling in transformed cells. b-catenin driven GFP expression in Src transformed mouse embryonic cells was decreased when cultured with cadherin competent nontransformed cells compared to transformed cells cultured with themselves, but not when cultured with cadherin deficient nontransformed cells. We also utilized a layered culture system to investigate the effects of oncogenic transformation and contact normalization on gene expression and oncogenic Src kinase mediated phosphorylation events. RNA-Seq analysis found that the cadherin dependent contact normalization inhibited the expression of 22 transcripts that were induced by Src transformation, and increased the expression of 78 transcripts that were suppressed by Src transformation. Phosphoproteomic analysis of cells expressing a temperature sensitive Src kinase construct found that contact normalization decreased phosphorylation of 10 proteins on tyrosine residues that were phosphorylated within 1 hour of Src kinase activation in transformed cells. Taken together, these results indicate that cadherin dependent contact normalization inhibits Wnt signaling to regulate oncogenic kinase activity and gene expression, particularly PDPN expression, in transformed cells in order to control tumor progression.

2024-02-19 | MSV000094121 | MassIVE

E-cadherin and EMT regulation by E47 transcription represor

Project description:Expression profile analysis in MDCK-E47 cells in comparisom with MDCK CMV control cells Keywords: Genetic Modification (overexpression of E-cadherin repressors)

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EGFR and E-cadherin coregulated genes mediate the growth and metastasis of gastric cancer cells by ceRNA networks

Project description:EGFR and E-cadherin are key genes closely related with gastric cancer. EGFR overexpression while E-cadherin deletion are characteristic partners in certain types of gastric cancer. Discovering their co-regulatory mechanisms will contribute to provide molecular basis and newer therapeutic strategy for this type of gastric cancer.In this study, E-cadherin overexpression and EGFR knockdown were performed in gastric cancer cells, and their effects on cell growth and metastasis were confirmed. Gene microarrays were used to analyze the changes of gene expression profile. A group of molecular targets co-regulated by EGFR and E-cadherin were found, including lncRNAs, circRNAs and mRNAs. Total 1204 DEGs are related to EGFR knockdown, while 3882 DEGs related to E-cadherin overexpression. Among their downregulated mRNAs, GLI2 and CEACAM6 were identical targets with most significance. Furthermore, 274 overlapping DEGs were screened as potential co-regulatory targets of EGFR and E-cadherin.With GLI2 and CEACAM6 as co-targets, we mapped two representative ceRNA networks to throw light on the co-regulation mechanism of EGFR and E-cadherin in regulating gastric cancer cells.

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Gene expression profile mediated by independent E-cadherin repressors

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Effect of E-cadherin by N-cadherin replacement in mouse intestinal epithelial cells

Project description:We conditionally substituted E-cadherin (E-cad; cadherin 1) with N-cadherin (N-cad; cadherin 2) during intestine development by generating mice in which an Ncad cDNA was knocked into the Ecad locus We used microarray to follow gene expression changes derived from lack of E-cadherin on intestinal epithelial cells

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E-cadherin interactome complexity and robustness resolved by quantitative proteomics

Project description:E-cadherin-mediated cell-cell adhesion and signaling plays an essential role in development and maintenance of healthy epithelial tissues. Adhesiveness mediated by E-cadherin is conferred by its extracellular cadherin domains and is regulated by an assembly of adaptors and enzymes associated with its cytoplasmic tail. Here, we used proximity biotinylation and quantitative proteomics to identify 561 proteins in the vicinity of E-cadherin’s cytoplasmic tail. Isolation of E-cadherin-mediated adhesion plaques from a cell-glass interface added positional context to the proteomic results. Moreover, using expression of GFP-tagged fusion proteins, we determine the subcellular localization of 83 of the E-cadherin proximal proteins, and identify 24 novel adherens junction components. We employed a structure-informed database of protein-protein interactions to construct a comprehensive E-cadherin interactome, containing 82 known and 419 previously uncharacterized proteins. Finally, we found that calcium chelation did not disrupt most protein interactions with E-cadherin, suggesting that most E-cadherin interactions are independent of cell-cell adhesion.

2016-07-06 | PXD000448 | Pride

Bulk RNA sequencing of VE-Cadherin+GFP+, VE-Cadherin- GFP+ and VE-Cadherin+GFP- populations from E11.5 miR144/451+/GFP mouse yolk sac.

Project description:The aim of the experiment was to compare a newly defined population VE-Cadherin+GFP+ to control populations, VE-Cadherin- GFP+ and VE-Cadherin+GFP-.

2019-04-20 | GSE113403 | GEO

Genes up-regulated by VE-cadherin expression and clustering at junctions

Project description:In 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.

2008-07-06 | GSE11674 | GEO

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