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Gene Expression Profiling on Stably Expressing Full Length (FL) JM-a CYT-1 or CYT-2 ERBB4 isoforms in MCF10A cells

ABSTRACT: Convergent and divergent effects of two FL ERBB4 isoforms on gene expression in normal-like MCF10A mammary epithelial cells lacking endogeneous ERBB4 expression. Control vector (VEC) and ERBB4 expression MCF10A cells(CYT1 or CYT2) were serum starved for 48 hours and incubated with or without ERBB4 ligand NRG1 for 2h. RNA samples were collected and analyzed.

ORGANISM(S): Homo sapiens

SUBMITTER: James Platt

PROVIDER: E-GEOD-57346 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene Expression Profiling on Stably Expressing ICD JM-a CYT-1 or CYT-2 ERBB4 isoforms in MCF10A cells

Project description:Convergent and divergent effects of two ICD ERBB4 isoforms on gene expression in normal-like MCF10A mammary epithelial cells lacking endogeneous ERBB4 expression. Control vector (VEC) and ERBB4 expression MCF10A cells (ICD CYT1 or CYT2) maintained in regular medium containing 10% serum, were collected and RNA samples were collected and analyzed.

2014-05-07 | E-GEOD-57339 | biostudies-arrayexpress

Characterizing gene expression changes that accompany succinate dehydrogenase subunit B (SDHB) RNA editing in monocyte-enriched peripheral blood mononuclear cell cultures

Project description:The goal of this study is to identify global changes in gene expression that accompany induction of site-specific RNA editing that targets the SDHB gene in monocyte-enriched peripheral blood mononuclear cell cultures. The results provide important information to understand the function of this programmed SDHB RNA mutation within the context of global gene expression changes that occur in cultured immune cells when the editing is induced. The study also specifically tests whether expression changes occur in SDH subunit genes, cytidine deaminase family of genes and hypoxia-inducible pathways. Overall design includes pairwise comparison of total gene expression profiles from uncultured cold-aggregated PBMCs (day 0), low-editing (culture day 3) and high-editing (culture days 5-8) samples, each from 4 donors. Submitted manuscript reported summary results from comparison of cultured low- and high-editing samples.

2013-04-10 | E-GEOD-45900 | biostudies-arrayexpress

In vitro knockdown of LAMP3 leads to down-regulation of interferon-inducible genes

Project description:We identified LAMP3 as a key driver gene of anti-viral subnetwork genes in cervical cancer patients. Therefore we tested this prediction using an in vitro system. This is the first direct demonstration of LAMP3 regulatory role in interferon-dependent immune response. We first pretreated HeLa cells with control siRNA or LAMP3 siRNA overnight and then added 1 ng/ml of interferon alpha to the cultures for 3 and 4 days

2011-12-29 | E-GEOD-29009 | biostudies-arrayexpress

expression of human and mouse breast cancer cell lines

Project description:Multiple breast cancer cell lines with different metastatic capabilities The goal of this study is to identify metastasis related genes in breast cancer We obtained RNA from each cell line using regular Trizol and RNA purification kit. Keywords: Expression profiling by array Multiple breast cancer cell lines with different metastatic capabilities

2011-01-15 | E-GEOD-25972 | biostudies-arrayexpress

Gene Array Analysis of Methylthioadenosine Supplementation in Dextran Sulfate Sodium Induced Colitis

Project description:Study hypothesized that oral supplementation of methylthioadenosine (MTA) would reduce the inflammatory response in mice exposed to an agent that induces colitis (DSS) and that this reduction in inflammatory response would lead to reduced clinical disease burden. Total RNA was collected from isolated colons of mice in the following treatment groups: untreated controls, DSS only, DSS+MTA

2011-12-20 | E-GEOD-34553 | biostudies-arrayexpress

TDP-43 loss of function inhibits endosomal trafficking and alters trophic signaling in neurons - Surface labelling

Project description:Nuclear clearance of TDP-43 into cytoplasmic aggregates is a key driver of neurodegeneration in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD), but the mechanisms are unclear. Here, we show that TDP-43 knockdown specifically reduces number and motility of RAB11-positive recycling endosomes in dendrites, while TDP-43 overexpression has the opposite effect. This is associated with delayed transferrin recycling in TDP-43 knockdown neurons and decreased 2-transferrin levels in patient CSF. Whole proteome quantification identified upregulation of the ESCRT component VPS4B upon TDP-43 knockdown in neurons. Luciferase report assays and chromatin immunoprecipitation suggest that TDP-43 represses VPS4B transcription. Preventing VPS4B upregulation or expression of its functional antagonist ALIX restores trafficking of recycling endosomes. Proteomic analysis revealed broad reduction in surface expression of key receptors upon TDP-43 knockdown including ErbB4, the neuregulin 1 receptor. TDP-43 knockdown delays surface delivery of ErbB4. ErbB4 overexpression, but not neuregulin 1 stimulation, prevents dendrite loss upon TDP-43 knockdown. Thus, impaired recycling of ErbB4 and other receptors to the cell surface may contribute to TDP-43 induced neurodegeneration by blocking trophic signaling.

2016-09-29 | PXD004744 | Pride

Microarray analysis of gene expression programm during cardiac development in contrasting rat strains SHRSP and F344

Project description:Reactivation of fetal gene expression patterns has been demonstrated to play a crucial role in common cardiac diseases in adult life including left ventricular (LV) hypertrophy (LVH). Thus, increased wall stress and neurohumoral activation are discussed to induce the return to expression of fetal genes after birth in LVH. We therefore aimed to test whether fetal gene expression programs are linked to the genetic predisposition to LVH. We performed genome-wide gene expression analysis by microarray-technology in a genetic rat model of LVH, i.e. the stroke-prone spontaneously hypertensive rat (SHRSP), to identify differences in expression patterns between day 20 of development (E20) and week 14 in comparison to a normotensive rat strain with low LV mass, i.e. Fischer (F344). 15232 probes from LV RNA from rats at week 14 and at E20 were detected as expressed (p < 0.05) and screened for differential expression. We identified 24 genes with a SHRSP specific up-regulation and 21 genes up-regulated in F344. Further bioinformatic analysis presented Efcab6, Ephx2 and Kcne1 as candidate genes for LVH that showed only in the hypertensive SHRSP rat a differential expression pattern during development and were significantly differentially expressed in adult SHRSP rats compared with two F344 and normotensive Wistar-Kyoto rats. They represent thus interesting novel targets for further functional analyses and the elucidation of mechanisms leading to LVH. Here we report a new approach to identify candidate genes for cardiac hypertrophy by analysing both gene expression differences between strains with contrasting cardiac phenotype and additionally the gene expression program during development. 26 samples for analysis; no replicates

2014-07-01 | E-GEOD-53512 | biostudies-arrayexpress

Molecular changes induced in melanoma cells by stromal cells and anti-BRAF therapy.

Project description:Tumor-associated stromal cells can enable cancer cells to become insensitive to therapy. They can promote aggressive phenotype in cancer cells, which become less responsive to drugs such as BRAF inhibitors (BRAFi) used to treat melanomas. To clarify potential mechanism behind stromal influence on melanoma, we analyzed gene expression in Melmet 5 melanoma cells grown as mono-cultures or co-cultures with lung fibroblasts with/without BRAFi. We have shown that Melmet 5 growing as co-cultures gained a de-differentiated, invasive transcriptional state, which is known to be linked to BRAFi-resistance. The transcriptional changes induced by BRAFi were much larger in Melmet 5 mono-cultures compared to co-cultures, indicating a much dampened transcriptional response to BRAFi in melanoma under the influence of fibroblasts. We conclude that interaction with the stromal cells stimulate melanoma cell transition to the invasive de-differentiated phenotype, leading to a worse response to BRAF inhibitors. Total RNA was isolated from Melmet 5 cell line growing as mono- or co-cultures with fibroblasts for 72 hours and treated with BRAFi for the last 24 hours.

2015-08-01 | E-GEOD-67637 | biostudies-arrayexpress

Co-regulated gene expression by estrogen receptor-M-NM-1 and liver receptor homolog-1 is a feature of the estrogen response in breast cancer cells

Project description:Estrogen receptor M-NM-1 (ERM-NM-1) is a nuclear receptor that is the driving transcription factor expressed in the majority of breast cancers. Recent studies have demonstrated that the liver receptor homolog-1 (LRH-1), another nuclear receptor, is ERM-NM-1-regulated in breast cancer cells. Further, LRH-1 stimulates proliferation and promotes motility and invasion of breast cancer cells. To determine the mechanisms of LRH-1 action in breast cancer cells, we carried out gene expression microarray analysis following siRNA-mediated LRH-1 knockdown. Interestingly, gene ontology (GO) category enrichment analysis of the genes differentially regulated in the presence or absence of LRH-1 identified estrogen responsive genes as the most highly enriched GO categories. To further define LRH-1 target genes, we performed chromatin immunoprecipitation coupled to massively parallel sequencing (ChIP-seq) to identify genomic targets of LRH-1. Remarkably, ChIP-seq showed LRH-1 binding at many ERM-NM-1 binding sites. Analysis of select binding sites confirmed regulation of ERM-NM-1-regulated genes by LRH-1 through binding to estrogen response elements, as exemplified by the TFF1/pS2 gene. Finally, LRH-1 over-expression stimulated ERM-NM-1 recruitment, whilst LRH-1 knockdown reduced ERM-NM-1 recruitment to ERM-NM-1 binding sites. Taken together, our findings establish a key role for LRH-1 in the regulation of ERM-NM-1 target genes in breast cancer cells and identify a mechanism in which co-operative binding of LRH-1 and ERM-NM-1 at estrogen response elements controls the expression of estrogen-responsive genes. MCF-7 cells were transfected with LRH-1 siRNA #2, #3, or with a non-targeting siRNA (siControl) for 72 hours. Following assessment of RNA integrity, four biological replicates for each siRNA treatment were used for microarray analysis.

2013-09-01 | E-GEOD-47803 | biostudies-arrayexpress

Genome-wide mapping of crossovers in all products of adult, single human female meioses reveals structural rearrangements of chromosomes and meiotic drive for recombinant chromatids

Project description:Meiotic recombination promotes genomic diversity by generating new combinations of alleles, while at the same time, maintaining genome stability by preventing chromosome missegregation and aneuploidy, such as Down Syndrome. We report here the first genome-wide maps of meiotic recombination in the human female meiosis. By utilizing information from all three meiotic products (oocyte, polar body 1 and polar body 2), our data reveal crossover rates that are in great excess (~40%) of recombination rate estimates from population-based studies. Recovery of all three meiotic products allowed us to identify structural defects to meiotic chromosomes that originate during meiosis, as well as true meiotic drive at meiosis II for the preferential exclusion of non-recombinant chromatids from the oocyte. Finally, we identify a novel chromosome segregation pattern reminiscent of 'inverted meiosis' that leads to chromosomally-balanced oocytes. The three products of meiosis from 13 oocytes and the gDNA from the five donors were analysed (total of 44 samples). Blank (negative) and positive (genomic DNA) control samples were provided for each DNA amplifiction run. No replicates were included as they were not available. No external references were included.

2015-03-01 | E-GEOD-53539 | biostudies-arrayexpress

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