Glutamine deprivation in U2OS cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE59931 | GEO | 2014/07/31
SECONDARY ACCESSION(S): PRJNA257073
REPOSITORIES: GEO
Similar Datasets
Project description:To understand the effects of glutamine deprivation on cell physiology we performed global analysis of gene expression in response to glutamine deprivation. U2OS cells were subjected to glutamine deprivation for 24h followed by RNA extraction and microarray analysis. U2OS cells were plated overnight followed by treatment for 24h with glutamine-containing and glutamine-depleted media. Three biological replicates were assayed for each condition.
2014-07-31 | E-GEOD-59931 | biostudies-arrayexpress
Project description:We applied the quantitative proteomics approach to estimate the relative abundance of proteins in HepG2 cells treated by glutamine deprivation. Two independent cultured cell lysates, namely control and glutamine deprivation, were marked with iTRAQ labels and subjected to LC-ESI-MS/MS analysis. The tryptic peptides of two samples were labeled with mass 113 (control) and 119 (glutamine deprivation) isobaric iTRAQ tags.
2016-02-09 | PXD003387 | Pride
Project description:We applied the quantitative proteomics approach to estimate the relative abundance of proteins in HepG2 cells treated by glutamine deprivation. Two independent cultured cell lysates, namely control and glutamine deprivation, were marked with iTRAQ labels and subjected to LC-ESI-MS/MS analysis. The tryptic peptides of two samples were labeled with mass 113 (control) and 119 (glutamine deprivation) isobaric iTRAQ tags.
2017-03-29 | MSV000080721 | MassIVE
Project description:There are two major subtype of cells in breast cancer. These cancer cells response differently to glutamine deprivation, here we use one luminal type of breast cancer cell (MCF7) and one basal type of breast cancer cell (MDAMB231) to compare the gene expression differences of these two types of cancer cells in glutamine deprivation. Many cancer cells depend on glutamine for survival and oncogenic transformation. Although targeting glutamine metabolism is proposed as novel therapies, their heterogeneity among different tumors is unknown. Here, we found only basal-type, but not luminal-type breast cancer cells, exhibited phenotypes of glutamine dependency and may benefit from glutamine-targeting therapeutics. The glutamine independence of luminal-type cells is caused by the specific expression of glutamine synthetase (GS), a pattern recapitulated in luminal breast cancers. The co-culture of luminal cells partially rescued the basal cells under glutamine deprivation, suggesting glutamine symbiosis. The luminal-specific expression of GS is directly induced GATA3 and down-regulates glutaminase expression to maintain subtype-specific glutamine metabolism. Collectively, these data indicate the distinct glutamine phenotypes among breast cells and enable the rational design of glutamine targeted therapies. Gene expression analysis in MCF7 and MDAMB231 cultured with or without glutamine for 24h
2012-01-01 | E-GEOD-26370 | biostudies-arrayexpress
Project description:There are two major subtype of cells in breast cancer. These cancer cells response differently to glutamine deprivation, here we use one luminal type of breast cancer cell (MCF7) and one basal type of breast cancer cell (MDAMB231) to compare the gene expression differences of these two types of cancer cells in glutamine deprivation. Many cancer cells depend on glutamine for survival and oncogenic transformation. Although targeting glutamine metabolism is proposed as novel therapies, their heterogeneity among different tumors is unknown. Here, we found only basal-type, but not luminal-type breast cancer cells, exhibited phenotypes of glutamine dependency and may benefit from glutamine-targeting therapeutics. The glutamine independence of luminal-type cells is caused by the specific expression of glutamine synthetase (GS), a pattern recapitulated in luminal breast cancers. The co-culture of luminal cells partially rescued the basal cells under glutamine deprivation, suggesting glutamine symbiosis. The luminal-specific expression of GS is directly induced GATA3 and down-regulates glutaminase expression to maintain subtype-specific glutamine metabolism. Collectively, these data indicate the distinct glutamine phenotypes among breast cells and enable the rational design of glutamine targeted therapies.
2012-01-01 | GSE26370 | GEO
Project description:Cancer cells heavily depend on the amino acid, glutamine, to meet the demands associated with growth and proliferation. Due to its rapid consumption, cancer cells frequently undergo glutamine starvation in vivo. We and others have shown that p53 is a critical regulator in metabolic stress resistance. To better understand the molecular mechanisms by which p53 activation promotes cancer cell adaptation to glutamine deprivation, we identified p53-dependent genes that are induced upon glutamine deprivation using RNA-seq analysis. We show that Slc7a3, an arginine transporter, is significantly induced by p53. We show the concomitant rise in intracellular arginine levels following glutamine deprivation is dependent on p53. The influx of arginine has minimal effect on known metabolic pathways upon glutamine deprivation. Instead, we found arginine serves as an effector for mTORC1 activation to promote in vitro and in vivo cell growth in response to glutamine starvation. Therefore, we identify a novel p53-inducible gene that contributes to the metabolic stress response.
2019-05-15 | GSE125782 | GEO
Project description:Glutamine deprivation enhances directed differentiation of renal organoids
| PRJNA529412 | ENA
Project description:Analysis of ovarian cancer cell line HeyA8 coculturing with cancer associated fibroblasts at gene expression level. The hypothesis test in this study is to show that cancer associated fibroblasts can influence the gene expression of HeyA8 under glutamine deprivation condition. Results provide important information of the response of HeyA8 when coculturing with cancer associated fibroblasts under glutamine deprivation, such as cell proliferation, apoptosis
2016-10-09 | GSE87773 | GEO
Project description:Purpose: The goal of this study is to examine gene expression regulation at the transcriptional and translational levels in response to various forms of nutrient deprivation, and whether there are differences between isogenic transformed and non-transformed cells. Mehods: We apply high-throughput sequencing of ribosome footprints (ribosome profiling) and poly(A) RNA (RNA sequencing) in an isogenic pair of transformed (tamoxifen-treated) and non-transformed (ethanol control) MCF10A-ER-Src cells subjected to the metabolic stresses that differentially affect global protein synthesis (Figure 1): deprivation of glutamine (for 30min and 4 hours), glucose (4hours), cysteine/cystine (4hours) or leucine/isoleucine/valine (brach-chain aminoacids - BCAA) (4hours). The same experiments were also performed in transformed ER-Src MCF10A treated with torin1 (500nM) for 4 hours. Results: Genome-wide translational profiling of glutamine deprived ER-Src MCF10A cells (for 30 minutes) shows increased translation of uORFs-containing mRNAs and down-regulation of ribosomal protein mRNAs, which is followed by increased translation and transcription of cytokine and inflammatory mRNAs (after 4 hours of glutamine deprivation). The transcription and translation of inflammatory and cytokine mRNAs is also stimulated in response to 4 hours deprivation of glucose, cysteine/cystine and BCAA, with the extent of stimulation correlating with the i) decrease in global protein synthesis and ii) down-regulation of all translationally-repressed mRNAs or ribosomal protein mRNAs. Conclusions: Pro-inflammatory gene expression is associated with translational repression in response to short-term nutrient deprivation.
2018-07-01 | GSE114794 | GEO