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

ABSTRACT: To investigate the TGFb pathway regulation on glycolysis in hPSCs, we processed glycolysis inhibition (2DG) treamtent in E7 medium (E8-TGFb) for 24h with or without multiple proteins of TGFb pathway in H1. Nodal, Activin A and TGFb were used for treatment with or without 2DG.

ORGANISM(S): Homo sapiens

PROVIDER: GSE247021 | GEO | 2025/05/05

REPOSITORIES: GEO

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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

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

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

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

2012-12-31 | GSE16816 | GEO

ERK5 sustains autocrine mitogenic balance for cell fate specification in human pluripotent stem cells [12h XMD RNA-seq]

Project description:To investigate the function ERK5 in the regulation of hPSC pluripotency, we processed ERK5 inhibition (XMD892) treamtent in E8 medium for 12hr in H1 ESCs.

2024-03-01 | GSE234057 | GEO

ERK5 sustains autocrine mitogenic balance for cell fate specification in human pluripotent stem cells [XMD RNA-seq]

Project description:To investigate the function ERK5 in the regulation of hPSC pluripotency, we processed ERK5 inhibition (XMD892) treamtent in E8 medium for 12/24/48hr in H1 ESCs.

2024-03-01 | GSE234163 | GEO

ERK5 sustains autocrine mitogenic balance for cell fate specification in human pluripotent stem cells [ChIP-seq]

Project description:To investigate the function ERK5 in the regulation of hPSC histone modification, we processed ERK5 inhibition (XMD892) treamtent in E8 medium for 24hr in H1 ESCs. And H3K27ac and H3K4me3 ChIP-seq test

2024-03-01 | GSE234055 | GEO

Proteomic response of yeast cells to 2-deoxyglucose exposure (0.2%, 2.5h)

Project description:Cancer cells display an altered metabolism with increased glycolysis and glucose uptake. Anti-cancer strategies targeting glycolysis through metabolic inhibitors have been considered. The glucose analog 2-deoxyglucose (2DG) is imported into cells and after phosphorylation becomes 2DG-6-phosphate, a toxic by-product that inhibits glycolysis. 2DG has other cellular effects and can induce resistance. Using yeast as a model, we performed an unbiased, mass-spectrometry-based approach to probe the cellular effects of 2DG on the proteome and study resistance mechanisms. We found that two 2DG-6-phosphate phosphatases, Dog1 and Dog2, were induced upon exposure to 2DG and participated in 2DG detoxication. 2DG induced Dog2 by activating several signaling pathways, such as the MAPK (the p38 ortholog Hog1)-based stress-responsive pathway, the unfolded protein response (UPR) triggered by 2DG-induced ER stress, and the MAPK (Slt2)-based cell wall integrity (CWI) pathway. Thus, 2DG-induced interference with cellular signaling rewired the expression of these endogenous phosphatases to promote 2DG resistance. Consequently, loss of the UPR or CWI pathways led to 2DG hypersensitivity. In contrast, DOG2 was transcriptionally repressed by glucose availability through the inhibition of the Snf1/AMPK pathway, and glucose-repression mutants were 2DG-resistant. The characterization and genome resequencing of spontaneous 2DG-resistant mutants revealed that DOG2 overexpression was a common strategy to achieve 2DG resistance. A human Dog2 homolog, HDHD1, also displays 2DG-6-phosphate phosphatase activity in vitro, and its overexpression conferred 2DG resistance in HeLa cells, suggesting potential interference with chemotherapies involving 2DG.

2019-09-09 | PXD014373 | Pride

Heterogeneity of Purkinje cells orchestrates cerebellar development.

Project description:In this study, we performed single-cell RNA sequencing of E6, E7, E8 and E9 chick cerebella to analyze diversity in in Purkinje cells during development.

2025-06-01 | GSE278923 | 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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