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Transcription profiling of human U87 wild type, neo-resistant and PDGF-A dominant negative U87 gliobastoma cells to identify PDGF-dependent patterns of gene expression

ABSTRACT: Overall study: Identification of PDGF-dependent patterns of gene expression in U87 glioblastoma cells. RNA was obtained from triplicate dishes of 5 different groups of U87 cells, each (total 15) analyzed with one U95 microarray chip.,Three different comparisons were made:,1) Clone 3.1 (34580-34582) vs. clone 3.3 (34583-34585) vs. parent U87 (34592-34594).,Purpose: demonstrate that the gene expression profiles between these 3 cell lines are not different, so they could be pooled as a single untreated group.,2) Pooled control group (34580-34585, 34592-34594) vs. clone 8.1 (34586-34588).,Purpose: identify genes specifically controlled by autocrine PDGF activity.,3) Clone 8.1 (34586-34588),vs. clone 8.1 treated with PDGF (34589-34591),Purpose: Identify genes specifically induced by exogenous PDGF.

ORGANISM(S): Homo sapiens

SUBMITTER: Ma D

PROVIDER: S-ECPF-GEOD-1923 | biostudies-other | 2005 Jul

REPOSITORIES: biostudies-other

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Transcription profiling of human U87 wild type, neo-resistant and PDGF-A dominant negative U87 gliobastoma cells to identify PDGF-dependent patterns of gene expression

Project description:Overall study: Identification of PDGF-dependent patterns of gene expression in U87 glioblastoma cells. RNA was obtained from triplicate dishes of 5 different groups of U87 cells, each (total 15) analyzed with one U95 microarray chip.,Three different comparisons were made:,1) Clone 3.1 (34580-34582) vs. clone 3.3 (34583-34585) vs. parent U87 (34592-34594).,Purpose: demonstrate that the gene expression profiles between these 3 cell lines are not different, so they could be pooled as a single untreated group.,2) Pooled control group (34580-34585, 34592-34594) vs. clone 8.1 (34586-34588).,Purpose: identify genes specifically controlled by autocrine PDGF activity.,3) Clone 8.1 (34586-34588),vs. clone 8.1 treated with PDGF (34589-34591),Purpose: Identify genes specifically induced by exogenous PDGF.

2007-12-12 | E-GEOD-1923 | biostudies-arrayexpress

Gene profiling: U87 IRE1 dominant negative cells vs. U87ctrl cells in culture

Project description:Transcriptome analysis was performed from human U87 glioblastoma cell clones: U87 IRE1.NCK DN (U87dn, IRE1 dominant negative) and U87 control (U87ctrl, empty plasmid). Cells were grown in DMEM supplemented with 10% FBS and glutamine for 16 hours in culture prior mRNA isolation and analyses U87dn cells expressing a dominant negative transgene of IRE1alpha were compared to U87ctrl cells transfected with the corresponding empty plamid to identify genes associated to tumor invasion and angiogenesis.

| S-ECPF-GEOD-22385 | biostudies-other

Gene profiling: U87 IRE1 dominant negative cells vs. U87ctrl cells in culture

2010-08-08 | GSE22385 | GEO

Gene profiling: U87 IRE1 dominant negative cells vs. U87ctrl cells in culture

2010-08-08 | E-GEOD-22385 | biostudies-arrayexpress

Identification of PDGF-dependent patterns of gene expression in U87 glioblastoma cells

Project description:Overall study: Identification of PDGF-dependent patterns of gene expression in U87 glioblastoma cells. RNA was obtained from triplicate dishes of 5 different groups of U87 cells, each (total 15) analyzed with one U95 microarray chip. Three different comparisons were made: 1) Clone 3.1 (34580-34582) vs. clone 3.3 (34583-34585) vs. parent U87 (34592-34594). Purpose: demonstrate that the gene expression profiles between these 3 cell lines are not different, so they could be pooled as a single untreated group. 2) Pooled control group (34580-34585, 34592-34594) vs. clone 8.1 (34586-34588). Purpose: identify genes specifically controlled by autocrine PDGF activity. 3) Clone 8.1 (34586-34588) vs. clone 8.1 treated with PDGF (34589-34591) Purpose: Identify genes specifically induced by exogenous PDGF. Keywords = platelet-derived growth factor Keywords = glioblastoma Keywords = brain cancer Keywords = sterol regulatory element binding protein Keywords = SREBP Keywords: ordered

2004-12-10 | GSE1923 | GEO

Dominant Cx26 mutants associated with hearing loss have dominant-negative effects on wild type Cx26.

Project description:Mutations in GJB2, the gene encoding the human gap junction protein connexin26 (Cx26), cause either non-syndromic hearing loss or syndromes affecting both hearing and skin. We have investigated whether dominant Cx26 mutants can interact physically with wild type Cx26. HeLa cells stably expressing wild type Cx26 were transiently transfected to co-express nine individual dominant Cx26 mutants; six associated with non-syndromic hearing loss (W44C, W44S, R143Q, D179N, R184Q, and C202F) and three associated with hearing loss and palmoplantar keratoderma (G59A, R75Q, and R75W). All mutants co-localized and co-immunoprecipitated with wild type Cx26, indicating that they interact physically, likely by forming admixed heteromeric/heterotypic channels. Furthermore, all nine mutants inhibited the transfer of calcein in cells stably expressing Cx26, demonstrating that they each have dominant effects on wild type Cx26. Taken together, these results show that dominant-negative effects of these Cx26 mutants likely contribute to the pathogenesis of hearing loss.

| S-EPMC3132585 | biostudies-literature

Expression profiling of ligand-stimulated wild type and tamoxifen-resistant MCF-7

Project description:Quantitative phosphoproteome and transcriptome analysis of ligand-stimulated MCF-7 human breast cancer cells was performed to understand the mechanisms of tamoxifen resistance at a systems level. Phosphoproteome data revealed that wild type (WT) cells were more enriched with phospho-proteins than tamoxifen-resistant (TamR) cells after stimulation with ligands. Surprisingly, decreased phosphorylation after ligand perturbation was more common than increased phosphorylation. In particular, 17beta-estradiol (E2) induced down-regulation in WT cells at a very high rate. E2 and the ErbB ligand, heregulin (HRG) induced almost equal numbers of up-regulated phospho-proteins in WT cells. Pathway and motif activity analyses using transcriptome data additionally suggested that deregulated activation of GSK3B　(glycogen synthase kinase 3 beta) and MAPK1/3 signaling might be associated with altered activation of CREB and AP-1 transcription factors in TamR cells and this hypothesis was validated by reporter assays. An examination of clinical samples revealed that, inhibitory phosphorylation of GSK3B at serine 9 was significantly lower in tamoxifen-treated breast cancer patients that eventually had relapses, implying that activation of GSK3B may be associated with the tamoxifen resistant phenotype. Thus, the combined phosphoproteome and transcriptome dataset analyses revealed distinct signal-transcription programs in tumor cells and provided a novel molecular target to understand tamoxifen resistance. The MCF-7 human breast cancer cell line and tamoxifen-resistant MCF-7 cells were stimulated by the growth hormone heregulin (HRG) or 17beta-estradiol (E2) in the presence or absence of tamoxifen. Control was set as non-treated cells.

| S-ECPF-GEOD-21618 | biostudies-other

Targeted point mutations of p53 lead to dominant-negative inhibition of wild-type p53 function.

Project description:The p53 tumor suppressor gene is the most frequently mutated gene in human cancers, and germ-line p53 mutations cause a familial predisposition for cancer. Germ-line or sporadic p53 mutations are usually missense and typically affect the central DNA-binding domain of the protein. Because p53 functions as a tetrameric transcription factor, mutant p53 is thought to inhibit the function of wild-type p53 protein. Here, we studied the possible dominant-negative inhibition of wild-type p53 protein by two different, frequently occurring point mutations. The R270H and P275S mutations were targeted into the genome of mouse embryonic stem cells to allow the analysis of the effects of the mutant proteins expressed in normal cells at single-copy levels. In embryonic stem cells, the presence of a heterozygous point-mutated allele resulted in delayed transcriptional activation of several p53 downstream target genes on exposure to gamma irradiation. Doxorubicin-induced apoptosis was severely affected in the mutant embryonic stem cells compared with wild-type cells. Heterozygous mutant thymocytes had a severe defect in p53-dependent apoptotic pathways after treatment with gamma irradiation or doxorubicin, whereas p53-independent apoptotic pathways were intact. Together these data demonstrate that physiological expression of point-mutated p53 can strongly limit overall cellular p53 function, supporting the dominant-negative action of such mutants. Also, cells heterozygous for such mutations may be compromised in terms of tumor suppression and response to chemotherapeutic agents.

| S-EPMC122453 | biostudies-literature

Transcription profiling of human sensitive and resistant tumours identify gene expression patterns in primary breast-cancer specimens that might predict response to taxanes

Project description:These patients proved resistant to docetaxel treatment, exhibiting residual tumor of 25% or greater remaining volume.

| S-ECPF-GEOD-349 | biostudies-other

Primary Osteocyte Supernatants Metabolomic Profiling of Two Transgenic Mice With Connexin43 Dominant Negative Mutants.

Project description:Osteocytes could release some small molecules (≤ 1 kDa) through gap junctions and hemichannels to extracellular environment, such as prostaglandin E2 (PGE2), nitric oxide (NO) and adenosine triphosphate (ATP), which play key roles in transferring signals between bone cells and other tissue cells. Connexin (Cx) 43 is the most abundant connexin in osteocytes. To further discover molecules released by osteocytes through Cx43 channels and better understand the regulatory function of Cx43 channels in osteocytes, we performed non-targeted global metabolomics analysis using liquid chromatography-tandem mass spectrometry (LC-MS/MS) on conditioned medium collected from osteocytes isolated from two transgenic mouse models with Cx43 dominant negative mutants driven by a 10 kb-DMP1 promoter: R76W (gap junctions are blocked, whereas hemichannels are promoted) and Δ130-136 (both gap junctions and hemichannels are blocked). The results revealed that several new categories of molecules, such as "fatty acyls" and "carboxylic acids and derivatives", could be released through osteocytic Cx43 channels. In addition, alteration of Cx43 channel function affected the release of metabolites related to inflammatory reaction and oxidative stress. Pathway analysis further showed that citric acid cycle was the most differential metabolic pathway regulated by Cx43 channels. In sum, these results isolated new potential metabolites released by osteocytes through Cx43 channels, and offered a novel perspective to understand the regulatory mechanisms of osteocytes on themselves and other cells as well.

| S-EPMC8169970 | biostudies-literature

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