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Glycolysis inhibition by 2-Deoxy-D-Glucose sustains a distinct cell pluripotency state in human pluripotency stem cells

ABSTRACT: Glycolysis inhibition by 2-Deoxy-D-Glucose sustains a distinct cell pluripotency state in human pluripotency stem cells

PROVIDER: PRJNA1035962 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26674256_1.fastq.gz	Fastqsanger.gz
	SRR26674256_2.fastq.gz	Fastqsanger.gz
	SRR26674257_1.fastq.gz	Fastqsanger.gz
	SRR26674257_2.fastq.gz	Fastqsanger.gz
	SRR26674258_1.fastq.gz	Fastqsanger.gz

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Glycolysis inhibition by 2-Deoxy-D-Glucose sustains a distinct cell pluripotency state in human pluripotency stem cells

Project description:To investigate the function glycolysis in the regulation of hPSC pluripotency, we processed glycolysis inhibition (2DG) treamtent in E8 medium for 5 cell passages in H1/H9 ESCs and NL1/NL4 hiPSCs.

2024-06-01 | GSE247041 | GEO

Modulation of immunomodulatory peptide activity by 2-deoxy-d-glucose

Project description:The goal of this study was to identify the role of glycolysis in the activity of immunomodulatory peptides with respect to macrophage function using the glycolytic inhibitor 2-deoxy-d-glucose

2016-10-29 | GSE74508 | GEO

Combinatorial targeting of glycolysis and oxidative phosphorylation suppresses tumor growth and metastases.

Project description:The Warburg effect, consisting of increased glucose uptake and glycolysis, provides metabolic energy as well as cellular building blocks for tumor growth. Inhibition of the Warburg effect with 2-deoxyglucose (2DG) has been explored in clinical trials with limited efficacy. Blockage of glycolysis can induce autopahgy resulting in alternative energy generation through oxidative phosphorylation providing a potential bypass of the effects of inhibition of glycolysis. Here in we demonstrate that activation of AMPK, as a consequence of energetic stress, induces mitochondrial energy production potentially bypassing the effects of glycolysis inhibition. We thus combined blockage of glycolysis by 2DG with inhibition of the electron transfer complex I (ETC1) in the mitochondria with the clinically applicable antidiabetic drug metformin. The combination resulted in activation of AMPK and autopahgy that however rendered eventual depletion of ATP and cell death. Furthermore, combined inhibition of glycolysis and mitochondrial respiration inhibited tumor growth and markedly decreased metastatic capacity in vivo. In order to understand the mechanism of these metabolic inhibitors, we performed whole genome transcriptional analysis. Human SK-4 esophageal cancer cell lines were treated with 5 different treatment groups [2 deoxy glucose (4mM), Metformin (5mM), AICAR (2mM), 2 deoxy glucose (4mM) plus Metformin (5mM) and 2 deoxy glucose (4mM) plus AICAR (2mM)] with non treated control groups for 12 hrs. Each groups was quadruplicated. Microarray experiments and data analysis were done at Dept. of Systems Biology, MDACC (Houston, USA)

2012-12-31 | E-GEOD-16816 | biostudies-arrayexpress

Proteomic analysis of mouse hearts treated with and without 2-deoxy-D-glucose

Project description:2-deoxy-D-glucose (2DG) is a glucose analog that is established to inhibit glucose metabolism via glycolysis. It has long been recognized as a potential chemical mimetic of calorie restriction, and it also has been shown to have anti-viral effects in infected cells, against among others SARS-CoV-2. This study aimed to determine whether intermittent treatment of mice with 2DG could alter nutrient metabolism in vivo and whether this would produce a proteomic signature of altered glucose metabolism and other cellular pathways, with a view to explaining the anti-viral properties of 2DG. Parallel physiological studies of the heart aimed to relate any proteomic changes to the function and performance of the heart, including assessing whether there were any signs of detrimental effects of 2DG.

2022-05-20 | PXD027974 | Pride

BRAF activation by metabolic stress promotes glycolysis and survival, sensitizing NRASQ61 mutated melanomas to targeted therapy.

Project description:NRAS-mutated melanoma lacks an approved first-line treatment. Metabolic reprogramming is considered a novel target to control cancer; however, it is mostly unknow how the NRAS oncogene contributes to this cancer hallmark. Here, we show that NRASQ61-mutated melanomas harbor specific metabolic alterations that render cells sensitive to sorafenib upon metabolic stress. Mechanistically, these cells seem to depend on glucose metabolism, as glucose deprivation promotes the switch of the RAF isoform used from CRAF to BRAF. This process contributes to cell survival and sustains glucose metabolism through the phosphorylation of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 2/6- phosphofructo-2-kinase/fructose-2,6-bisphosph 3 (PFKFB2/PFKFB3) heterodimers by BRAF. In turn, this phosphorylation favors the allosteric activation of phosphofructokinase-1 (PFK1), generating a feedback loop linking glycolysis and the RAS signaling pathway. In vivo treatment of NRASQ61 mutant melanomas, including patient-derived xenografts, with the combination of 2-deoxy-D-glucose (2-DG) and sorafenib effectively inhibits tumor growth. Thus, we provide evidence of the contributions of NRAS oncogenes to metabolic rewiring and proof of principle for the treatment of NRAS-mutated melanoma with combinations of metabolic stress (glycolysis inhibitors) and already approved drugs such as sorafenib.

2023-01-09 | PXD028297 | Pride

Deep sequencing of endogenous mRNA from Caenorhabditis elegans in the presence of 2-deoxy-D-glucose (DOG) at 4 different time points

Project description:Background: C. elegans fed with a chemical inhibitor of glucose, namely 2-deoxy-D-glucose (DOG), exhibit considerably extended life span. DOG, in contradiction to D-glucose, cannot be metabolized in the glycolytic pathway. This results in the fact that less glucose is available for ATP production, and thus makes DOG-feeding of the roundworms equivalent to glucose restriction. The RNA-seq data comprises 4 age groups (1, 5, 10 and 20 days after L4) Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)

2013-11-06 | GSE46344 | GEO

Microarray analysis of regulatory and inflammatory macrophages differentiated with glycolysis inhibitor

Project description:The gene expression patterns of macrophages were analyzed to understand how glycolysis inhibitor affects macrophage differentiation. Human monocytes derived from peripheral blood were cultured in vitro in the presence of macrophage colony-stimulating factor (M-CSF) to yield regulatory macrophages (M-Mφs), or M-CSF plus interferon-gamma to yield inflammatory macrophages (Mγ-Mφs). 2-deoxy-D-glucose (2-DG), a glycolysis inhibitor, was added during macrophage differentiation. Gene expression patterns of monocytes, M-Mφs and Mγ-Mφs diffrentiated with or without 2-DG were analyzed by microarray analysis.

2016-03-07 | GSE74182 | GEO

Deep sequencing of endogenous mRNA from Caenorhabditis elegans in the presence of 2-deoxy-D-glucose (DOG) at 4 different time points

Project description:Background: C. elegans fed with a chemical inhibitor of glucose, namely 2-deoxy-D-glucose (DOG), exhibit considerably extended life span. DOG, in contradiction to D-glucose, cannot be metabolized in the glycolytic pathway. This results in the fact that less glucose is available for ATP production, and thus makes DOG-feeding of the roundworms equivalent to glucose restriction. The RNA-seq data comprises 4 age groups (1, 5, 10 and 20 days after L4) 11 samples: mRNA profiles of 1-day, 5-day and 10-day old worms as triplicates for DOG treatment; mRNA profiles of 20-day old worms as duplicates for DOG treatment

2013-11-06 | E-GEOD-46344 | biostudies-arrayexpress

Glucose supply and glycolysis inhibition shape the clinical fate of preterm newborns infected with Staphylococcus epidermidis [whole blood]

Project description:To investigate if appropriately adjusted parenteral glucose supply and/or temporary glycolysis inhibition by administration may help to prevent sepsis or improve sepsis outcomes of preterm newborns, we using a preterm pig model inoculated with Staphylococcus epidermidis to mimic the inflammation condition of preterm newborns at birth and treated them with different parenteral nutrition glucose supplyment and glycolysis inhibitor administration. We then performed gene expression profiling analysis using data obtained from RNA-seq of preterm pigs` whole blood, which collected at 12 hours after SE infection, treated with different parenteral glucose supply and glycolysis inhibitor administration.

2022-06-29 | GSE201552 | GEO

Targeting glycolysis reduces infection and dampens inflammation in a host-directed therapy for dengue

Project description:Monocytes are the key mediators of inflammatory responses in virus patients, and are also the only blood cell type that supports productive infection both in vitro and in vivo. In this study, we assessed how dengue infection alters the metabolic response of monocytes and affects ensuing inflammatory mechanisms. Using a glycostress assay, we showed that in vitro infected primary human monocytes by dengue virus and monocytes isolated from thrombocytopenic dengue patients, during critical stage of the disease, had increased glycolysis. Single cell transcriptomics revealed an enhanced expression of interferon-related genes and glycolytic genes in classical and intermediate monocytes of dengue patients with more pronounced thrombocytopenia. Targeting glycolysis by 2-deoxy-glucose (2DG) reduced dengue infection and dampened pro-inflammatory cytokines in monocytes, both in vitro and in mouse models. Collectively, these results suggest that glycolysis could be a possible target for pharmaceutical intervention to regulate pathogenic host responses in dengue.

2021-04-02 | GSE171290 | GEO

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