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Transcription profiling by array of human SKBR-3 cells VE-cadherin siRNA and then treated with retinoic acid

ABSTRACT: SKBR-3 cells were transfected with Luciferase siRNA or VE-cadherin siRNA and then treated with 10-7M retinoic acid (RA) for 48 hours.

ORGANISM(S): Homo sapiens

SUBMITTER: Prahalad P

PROVIDER: S-ECPF-MEXP-2418 | biostudies-other | 2010

REPOSITORIES: biostudies-other

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Transcription profiling by array of human SKBR-3 cells VE-cadherin siRNA and then treated with retinoic acid

Project description:SKBR-3 cells were transfected with Luciferase siRNA or VE-cadherin siRNA and then treated with 10-7M retinoic acid (RA) for 48 hours.

2010-03-13 | E-MEXP-2418 | biostudies-arrayexpress

Transcription profiling by array of human BT-20 cells with siRNA silencing of E-cadherin and P-cadherin

Project description:Gene expression of four cell lines derived from BT-20 cells, namely, BT20 siCtr (E+/P+), BT20 siPcad (E+/P-), BT20 siEcad (E-/P+), and BT20 siEPcad (E-/P-) was compared using Agilent Human GE 4x44k v2 Microarrays and the Agilent One-Color Microarray-Based Gene Expression Analysis protocol (Quick Amp Labeling kit). Three independent biological samples were obtained for each cell line and BT20 siCtr (E+/P+) cells were used as control for data analysis.

| S-ECPF-MEXP-3329 | biostudies-other

Role of Sox-9, ER81 and VE-cadherin in retinoic acid-mediated trans-differentiation of breast cancer cells.

Project description:Many aspects of development, tumor growth and metastasis depend upon the provision of an adequate vasculature. This can be a result of regulated angiogenesis, recruitment of circulating endothelial progenitors and/or vascular trans-differentiation. The present study demonstrates that treatment of SKBR-3 breast cancer cells with retinoic acid (RA), an important regulator of embryogenesis, cancer and other diseases, stimulates the formation of networks in Matrigel. RA-treatment of SKBR-3 cells co-cultured with human umbilical vein endothelial cells resulted in the formation of mixed structures. RA induces expression of many endothelial genes including vascular endothelial (VE) cadherin. VE-cadherin was also induced by RA in a number of other breast cancer cells. We show that RA-induced VE-cadherin is responsible for the RA-induced morphological changes. RA rapidly induced the expression of Sox-9 and ER81, which in turn form a complex on the VE-cadherin promoter and are required to mediate the transcriptional regulation of VE-cadherin by RA. These data indicate that RA may promote the expression of endothelial genes resulting in endothelial-like differentiation, or provide a mechanism whereby circulating endothelial progenitor cells could be incorporated into a growing organ or tumor.

| S-EPMC2444023 | biostudies-literature

Transcription profiling by array of human SKBR-3 cells after treatment with retinoic acid

Project description:SKBR-3 cells were treated with control or 0.1uM RA for 48 hours

| S-ECPF-MEXP-2417 | biostudies-other

Retinoic acid mediates regulation of network formation by COUP-TFII and VE-cadherin expression by TGFbeta receptor kinase in breast cancer cells.

Project description:Tumor development, growth, and metastasis depend on the provision of an adequate vascular supply. This can be due to regulated angiogenesis, recruitment of circulating endothelial progenitors, and/or vascular transdifferentiation. Our previous studies showed that retinoic acid (RA) treatment converts a subset of breast cancer cells into cells with significant endothelial genotypic and phenotypic elements including marked induction of VE-cadherin, which was responsible for some but not all morphological changes. The present study demonstrates that of the endothelial-related genes induced by RA treatment, only a few were affected by knockdown of VE-cadherin, ruling it out as a regulator of the RA-induced endothelial genotypic switch. In contrast, knockdown of the RA-induced gene COUP-TFII prevented the formation of networks in Matrigel but had no effect on VE-cadherin induction or cell fusion. Two pan-kinase inhibitors markedly blocked RA-induced VE-cadherin expression and cell fusion. However, RA treatment resulted in a marked and broad reduction in tyrosine kinase activity. Several genes in the TGFbeta signaling pathway were induced by RA, and specific inhibition of the TGFbeta type I receptor blocked both RA-induced VE-cadherin expression and cell fusion. Together these data indicate a role for the TGFbeta pathway and COUP-TFII in mediating the endothelial transdifferentiating properties of RA.

| S-EPMC2850308 | biostudies-literature

Transcription profiling by array of human MCF cells treated with estrogen

Project description:The estrogen receptor is the master transcriptional regulator of breast cancer phenotype and the archetype of a molecular therapeutic target. We mapped all estrogen receptor and RNA polymerase II binding sites on a genome-wide scale, identifying the authentic cis binding sites and target genes, in breast cancer cells. Combining this unique resource with gene expression data demonstrates distinct temporal mechanisms of estrogen-mediated gene regulation,particularly in the case of estrogen-suppressed genes. Furthermore, this resource has allowed the identification of cis-regulatory sites in previously unexplored regions of the genome and the cooperating transcription factors underlying estrogen signaling in breast cancer. Experiment Overall Design: This Series currently contains the gene expression data accompaning Carroll JS et al. Nature Genetics 38,1289-1297(2006). MCF7 cells were stimulated with 100 nM estrogen for 0, 3, 6, or 12h. All experiments were performed in triplicate.

| S-ECPF-GEOD-11324 | biostudies-other

Transcription profiling by array of human breast cancer cell lines treated with HPGD targeting siRNA and shRNA

Project description:Effects of siRNA and shRNA treatment on gene expression in breast cancer cell lines

| S-ECPF-TABM-1162 | biostudies-other

Transcription profiling by array of human T98G cells treated with doxycycline to induce expression of EGFP-CD44ICD in cells transfected with control or HIF2A siRNA

Project description:T98G cells treated (or not) with Doxycycline to induce expression of EGFP-CD44ICD in cells transfected with control or HIF2A siRNA.

| S-ECPF-MEXP-3914 | biostudies-other

Transcription factor Erg regulates angiogenesis and endothelial apoptosis through VE-cadherin.

Project description:Tight regulation of the balance between apoptosis and survival is essential in angiogenesis. The ETS transcription factor Erg is required for endothelial tube formation in vitro. Inhibition of Erg expression in human umbilical vein endothelial cells (HUVECs), using antisense oligonucleotides, resulted in detachment of cell-cell contacts and increased cell death. Inhibition of Erg expression by antisense in HUVECs also lowered expression of the adhesion molecule vascular endothelial (VE)-cadherin, a key regulator of endothelial intercellular junctions and survival. Using chromatin immunoprecipitation, we showed that Erg binds to the VE-cadherin promoter. Furthermore, Erg was found to enhance VE-cadherin promoter activity in a transactivation assay. Apoptosis induced by inhibition of Erg was partly rescued by overexpression of VE-cadherin-GFP, suggesting that VE-cadherin is involved in the Erg-dependent survival signals. To show the role of Erg in angiogenesis in vivo, we used siRNA against Erg in a Matrigel plug model. Erg inhibition resulted in a significant decrease in vascularization, with increase in caspase-positive endothelial cells (ECs). These results identify a new pathway regulating angiogenesis and endothelial survival, via the transcription factor Erg and the adhesion molecule VE-cadherin.

| S-EPMC2275018 | biostudies-literature

Transcription profiling by array of human U251 cells treated with DMSO or enzastaurin

Project description:We identified GSK3 as a regulator of GBM cell survival using microarray analysis, small molecule and genetic inhibitors of GSK3 activity. Various molecular and genetic approaches were then employed to dissect out the molecular mechanisms responsible for GSK3 inhibition-induced cytotoxicity. Experiment Overall Design: RNA extracted from U251 cells treated with DMSO or Enzastaurin for indicated time were hybridized to Affymetrix expression arrays (HG_U133-Plus_2) to detect changes in gene expression caused by Enzastaurin. Three replicates per sample were used.

| S-ECPF-GEOD-11285 | biostudies-other

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