Microarray of human lung cancer cell line A549 treated with glucosamine against untreated controls
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER:
PROVIDER: E-MTAB-14871 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Examined the expression effects of supplementing Drosophila food on heart and nephrocyte complexes 30 female flies fed standard diet supplemented with 0.1 M glucosamine were dissected in cold ADH, and heart/nephrocyte complexes were harvested and analyzed. Animals were pre-fed glucosamine or sucrose, and heart/nephrocyte complexes were assessed for differences in gene expression.
2015-06-12 | E-GEOD-69815 | biostudies-arrayexpress
Project description:We did transcription profiling on the effect of glucosamine in Saccharomyces cerevisiae using Research Genetics strains BY4741 (wild type) and 5251 (fks1). Yeast cells exposed to glucosamine in YPD growth medium show a significant increase in chitin content in the lateral cell wall. Likewise, cell wall stress caused by a gene deletion e.g., fks1 also results in elevated chitin. By comparing our data for fks1 with those from the literature we confirmed a strong induction of genes responsive to cell wall integrity, environmental stress as well as genes involved in cell signaling. Wild type cells treated with 15 mM glucosamine for 2 hours did not show any significant change in their transcription profile although the chitin level doubled during this time. For cells continuously exposed to glucosamine (steady state) there was a moderate transcription response, 105 genes showed a two-fold or higher change. The largest groups of up-regulated genes were those involved in mating, sporulation and cell cycle arrest. The largest group of down-regulated genes pertained to mitochondrial respiration. There was little overlap between those genes that have altered transcription from glucosamine treatment and those responsive to the fks1 mutation.
2007-07-07 | E-GEOD-441 | biostudies-arrayexpress
Project description:Glucosamine proved to be a potent, broad-spectrum inhibitor of IL-1beta. Of the 2,813 genes whose transcription was altered by IL-1beta stimulation (p<0.0001), glucosamine significantly blocked the response in 2,055 (~73%). Glucosamine fully protected the chondrocytes from IL-1-induced expression of inflammatory cytokines, chemokines and growth factors as well as proteins involved in PGE2 and NO synthesis. It also blocked the IL-1-induced expression of matrix specific proteases such as MMPs -3,-9,-10,-12 and ADAMTS-1. Experiment Overall Design: Articular cartilage was isolated from the femoral heads of male Wistar rats under aseptic conditions. Chondrocytes were obtained by sequential digestion of the cartilage with pronase and type II collagenase. After filtration to remove tissue debris, the cells were cultured in 75-cm2 flasks in complete Dulbeccoâs Modified Eagle Medium (DMEM; supplemented with 10% fetal bovine serum and 1% penicillin-streptomycin at 37°C in a humidified atmosphere containing 5% CO2. Experiments were subsequently performed with second-passage cultures whereby the cells from the large cultures were trypsinized, pooled and seeded into twenty 25 cm2 flasks. These were then divided into 4 treatment groups to evaluate the effects of glucosamine and IL-1 on global transcription patterns.To the culture medium in half of the flasks, glucosamine, HCl was added to a final concentration of 20 mM. Six hours later, IL-1beta was added at 10 ng/ml to 5 of the flasks receiving glucosamine and to 5 of the untreated flasks. Fourteen hours post IL-1beta stimulation, total RNA was isolated individually from the respective cultures and microarray experiments processed.
2009-04-23 | E-GEOD-6119 | biostudies-arrayexpress
Project description:We performed single-cell RNA sequencing of multiple IGF-1R loss-of function mouse mammary tumor models to uncover how IGF-1R signaling regulates intrinsic epithelial cell signaling to suppress metastasis. We identify key pathways necessary for promoting metastasis, determined IGF-1R is required to maintain a metastatic suppressive tumor microenvironment and demonstrate that attenuated epithelial IGF-1R signaling in the MMTV-Wnt1 mouse tumor model is sufficient for metastatic invasion. We further show that adherence between luminal and basal tumor cells is necessary for tumor growth at the secondary site and that reduced IGF-1R signaling in tumor epithelial cells inhibits secondary tumor epithelial cell growth due to dysregulated E-cadherin and P-cadherin and loss of cell-cell adhesion.
2022-11-21 | GSE182236 | GEO
Project description:We did transcription profiling on the effect of glucosamine in Saccharomyces cerevisiae using Research Genetics strains BY4741 (wild type) and 5251 (fks1). Yeast cells exposed to glucosamine in YPD growth medium show a significant increase in chitin content in the lateral cell wall. Likewise, cell wall stress caused by a gene deletion e.g., fks1 also results in elevated chitin. By comparing our data for fks1 with those from the literature we confirmed a strong induction of genes responsive to cell wall integrity, environmental stress as well as genes involved in cell signaling. Wild type cells treated with 15 mM glucosamine for 2 hours did not show any significant change in their transcription profile although the chitin level doubled during this time. For cells continuously exposed to glucosamine (steady state) there was a moderate transcription response, 105 genes showed a two-fold or higher change. The largest groups of up-regulated genes were those involved in mating, sporulation and cell cycle arrest. The largest group of down-regulated genes pertained to mitochondrial respiration. There was little overlap between those genes that have altered transcription from glucosamine treatment and those responsive to the fks1 mutation. Keywords = saccharomyces chitin glucosamine Keywords: parallel sample
2003-05-30 | GSE441 | GEO
Project description:Transcriptional profiles of Escherichia coli MG1655 in mixed culture with Pseudomonas aeruginosa PAO1 showed a number of E. coli genes to be upregulated including purA-F and other genes associated with purine synthesis. In contrast, genes associated with pyrimidine synthesis were unaffected. Competition experiments in both planktonic and biofilm cultures, using three purine synthesis mutants, purD, purH, and purT showed little difference in E. coli survival from the parent strain. As purines are components of the cell signals, cAMP and c-di-GMP, we conducted competition experiments with E. coli mutants lacking adenylate cyclase (cyaA), cAMP phosphodiesterase (cpdA), and the catabolite receptor protein (crp), as well as ydeH, an uncharacterized gene that has been associated with c-di-GMP synthesis. Survival of the cyaA and crp mutants during co-culture were significantly less than the parent strain. Supplementation of the media with 1mM cAMP could restore survival of the cyaA mutant but not the crp mutant. In contrast, survival of the cpdA mutant was similar to the parent strain. Survival of the ydeH mutant was moderately less than the parent, suggesting that cAMP has more impact on E. coli mixed culture growth than c-di-GMP. Addition of 1 mM indole restored the survival of both the cyaA and crp mutations. Mutants in genes for tryptophan synthesis (trpE) and indole production (tnaA) showed a loss of competition and recovery through indole supplementation, comparable to the cyaA and crp mutants. Overall, these results suggest indole and cAMP as major contributing factors to E. coli growth in mixed culture. E. coli MG1655 and P. aeruginosa PAO1 were grown in a minimal defined medium containing N-acetyl glucosamine, overnight at 37C to an OD of 1.5, and then inoculated in fresh media at an OD of 0.001 and grown in pure or mixed culture for 4-5 hours to a final OD of 0.5. RNA was extracted, purified, reverse transcribed to cDNA and then analyzed on E. coli and P. aeruginosa chips from Affymetrix. Expression profiles of mixed culture-grown organisms were compared to pure culture E. coli and P. aeruginosa grown on the same defined medium.
2011-11-29 | E-GEOD-26932 | biostudies-arrayexpress
Project description:The important role of IGF-1R in cancers has been well established. Classical model involves IGF-1/2 binding to IGF-1R, following activation of the PI3K/Akt pathway, thereby promoting cell proliferation, apoptosis inhibition and treatment resistance. While IGF-1R has become a promising target for cancer therapy, clinical disclosures subsequently have been less encouraging. The question is whether targeting IGF/IGF-1R still holds therapeutic potential. Here we show a novel mechanism that knockdown IGF-1R surprisingly triggers cytoplasmic viral RNA sensors MDA5 and RIG-1, leading to mitochondrial apoptosis in cancer. We analyzed MDA5 and RIG-1 in the intestinal epithelium of IGF-1R knockdown mice. Igf1r+/- mice demonstrated higher MDA5 and RIG-1 than WT mice. IGF-1R knockdown-triggered MDA5 and RIG-1 was further analyzed in human cancer and normal cells. Increased MDA5 and RIG-1 were clearly seen in the cytoplasm identified by immunofluoresce in the cells silenced IGF-1R. Block off IGF-1R downstream PI3K/Akt did not impact on MDA5 and RIG-1 expression. IGF-1R knockdown-triggered MDA5 and RIG-1 and their signaling pathways were similar to those of viral RNA mimetic poly(I:C) had. IGF-1R knockdown-triggered MDA5 and RIG-1 led to cancer apoptosis through activation of the mitochondrial pathway. In vivo assay, Igf1r+/- mice strongly resisted AOM-induced colonic tumorigenesis through triggering MDA¬5- and RIG-1-mediated apoptosis. Notably, RIG-I and MDA5-mediated proapoptotic signaling pathway is preferential active in cancer cells. These data suggest that targeting IGF-1R-triggered MDA5 and RIG-1 might have therapeutic potential for cancer treatment.
2019-11-30 | GSE122534 | GEO
Project description:Define regulated genes upon 24 hours of glucosamine treatment in KMH2 and Ramos
2014-08-18 | GSE49185 | GEO
Project description:The insulin-like growth factor 1 receptor (IGF-1R) plays crucial roles in developmental and cancer biology. Most of its biological effects have been ascribed to its tyrosine kinase activity. We report that IGF-1 promotes the modification of IGF-1R by small ubiquitin-like modifier protein-1 (SUMO-1) and its translocation to the nucleus. Nuclear IGF-1R associated with enhancer-like elements and increased transcription in reporter assays. We used ChIP-seq to examine the interaction of IGF-1R with DNA on a genome-wide scale. Analysis of the data set resulted in 568 candidate peaks, that is, statistically significant IGF-1R-enriched regions. The IGF-1R-enriched regions were divided into five classes on the basis of their location relative to known genes. Most of the IGF-1R-interacting sites (80%) were located distal from any annotated gene (intergenic), 6.3% were located in introns, 6.3% in exons, 3.4% were <20 kb upstream of an annotated transcript start site (5'UTR + 20 kb upstream), and 3.6% were <20 kb downstream of an annotated transcript end site (3'UTR + 20 kb downstream).
2010-08-25 | GSE23792 | GEO
Project description:The insulin-like growth factor 1 receptor (IGF-1R) plays crucial roles in developmental and cancer biology. Most of its biological effects have been ascribed to its tyrosine kinase activity. We report that IGF-1 promotes the modification of IGF-1R by small ubiquitin-like modifier protein-1 (SUMO-1) and its translocation to the nucleus. Nuclear IGF-1R associated with enhancer-like elements and increased transcription in reporter assays. We used ChIP-seq to examine the interaction of IGF-1R with DNA on a genome-wide scale. Analysis of the data set resulted in 568 candidate peaks, that is, statistically significant IGF-1R-enriched regions. The IGF-1R-enriched regions were divided into five classes on the basis of their location relative to known genes. Most of the IGF-1R-interacting sites (80%) were located distal from any annotated gene (intergenic), 6.3% were located in introns, 6.3% in exons, 3.4% were <20 kb upstream of an annotated transcript start site (5'UTR + 20 kb upstream), and 3.6% were <20 kb downstream of an annotated transcript end site (3'UTR + 20 kb downstream). Analysis of the genomic interaction of IGF1R in DFB cells
2010-08-25 | E-GEOD-23792 | biostudies-arrayexpress