Ontology highlight
ABSTRACT:
PROVIDER: PRJNA860360 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20324952_1.fastq.gz | Fastqsanger.gz | |||
| SRR20324952_2.fastq.gz | Fastqsanger.gz | |||
| SRR20324953_1.fastq.gz | Fastqsanger.gz | |||
| SRR20324953_2.fastq.gz | Fastqsanger.gz | |||
| SRR20324954_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Solute carrier family 7 member 11 (SLC7A11; also known as xCT) is a cystine transporter frequently overexpressed in cancers. Cancer cells with high expression of SLC7A11 (SLC7A11high) are resistant to ferroptosis but exquisitely sensitive to glucose deprivation-induced cell death, although the underlying mechanism of the latter cell death remains poorly understood. Here we show that
We found that glucose deprivation induced a novel type of cell death in SLC7A11high cancer cells that was different from apoptosis or ferroptosis. And the bioorthogonal chemical proteomics analysis revealed that a large amount of actin cytoskeleton proteins were shown with significantly dysregulated disulfides induced by glucose starvation in SLC7A11high cancer cells. In mechanism, SLC7A11high mediated cystine uptake and subsequent reduction to cysteine forced disulfide stress on actin cytoskeleton upon glucose deprivation through draining intracellular reduced nicotinamide adenine dinucleotide phosphate (NADPH) pool, which was independent of generating reactive oxygen species (ROS). The disulfide stress on the actin cytoskeleton induced rapidly contracted actin filaments and detached from the plasma membrane, which incurred cell death. In the end, using whole-genome CRISPR/Cas9 knock-out screening we identified NCKAP1 as a downstream factor of SLC7A11 to promoting cell death upon glucose deprivation by inhibiting branched actin filaments.
| MSV000088066 | MassIVE
Project description:<h4><strong>OBJECTIVE:</strong> Emerging evidence suggests that glucose depletion (GD)-induced cell death depends on system Xc-, a glutamate/cystine antiporter extensively studied in ferroptosis. However, the underlying mechanism remains debated. Our study confirmed the correlation between system Xc- and GD-induced cell death and provided a strategic treatment for oral squamous cell carcinoma (OSCC).</h4><p><strong>METHODS:</strong> qPCR and Western blotting were performed to detect changes in xCT and CD98 expression after glucose withdrawal. Then, the cell viability of OSCCs under the indicated conditions was measured. To identify the GD-responsible transcriptional factors of SLC7A11, we performed a luciferase reporter assay and a ChIP assay. Further, metabolomics was conducted to identify changes in metabolites. Finally, mitochondrial function and ATP production were evaluated using the seahorse assay, and NADP+/NADPH dynamics were measured using a NADP+/NADPH kit.</p><p><strong>RESULTS:</strong> In OSCCs, system Xc- promoted GD-induced cell death by increasing glutamate consumption, which promoted NADPH exhaustion and TCA blockade. Moreover, GD-induced xCT upregulation was governed by the p-eIF2α/ATF4 axis.</p><h4><strong>CONCLUSIONS:</strong> System Xc- overexpression compromised the metabolic flexibility of OSCC under GD conditions, and thus, glucose starvation therapy is effective for killing OSCC cells.</h4>
2024-01-16 | MTBLS5358 | MetaboLights
Project description:Little is known about regulation of gene activity of the major pathogen Staphylococcus aureus during actual human infection. Here we characterize the transcriptome using deep RNA sequencing and the metabolome using NMR of S. aureus infected joint fluid derived from an acute human prosthetic joint infection, and compare them with the genome, transcriptome and metabolome of an isolate obtained from the sample grown in vitro (LB medium). The transcriptome indicated that the bacterial infection sustained on a versatile human-cell-based diet consisting of amino acids, glycans and nucleosides, since significant upregulation of genes involved in the catabolic degradation pathways of these compounds were observed in situ. This is consistent with metabolite analysis of the infected joint fluid and of S. aureus culture supernatants where the concentration of most amino acids and some amino sugars were found to be higher in the joint fluid, whereas the concentration of glucose was higher in culture supernatant. Furthermore, presumably because of oxygen limitations in the joint fluid, transcriptomic evidence for fermentation was observed, consistent with the presence of fermentation products (ethanol) in situ. Moreover, many, but not all, of the known virulence factor genes were upregulated in situ as well as the nine genes encoding the iron uptaking siderophore synthesis system.
2015-10-01 | GSE62091 | GEO
Project description:Glucose deprivation induced gene expression
| PRJNA668528 | ENA
Project description:Ferroptosis is a form of regulated cell death that can be induced by inhibition of the cystine-glutamate antiporter, system xc-. Among the existing system xc- inhibitors, imidazole ketone erastin (IKE) is a potent, metabolically stable inhibitor of system xc- and inducer of ferroptosis potentially suitable for in vivo applications. We investigated the pharmacokinetic and pharmacodynamic features of IKE in a diffuse large B cell lymphoma (DLBCL) xenograft model and demonstrated that IKE exerted an antitumor effect by inhibiting system xc-, leading to glutathione depletion, lipid peroxidation, and the induction of ferroptosis biomarkers both in vitro and in vivo. Using untargeted lipidomics and qPCR, we identified distinct features of lipid metabolism in IKE-induced ferroptosis. In addition, biodegradable polyethylene glycol-poly(lactic-co-glycolic acid) nanoparticles were employed to aid in IKE delivery and exhibited reduced toxicity compared with free IKE in a DLBCL xenograft model.
2019-04-17 | MTBLS774 | MetaboLights
Project description:Knockdown of YAP in HCT116 cells by lentivirus-mediated shRNA, and after glucose deprivation treatment using total RNA for sequencing analysis to evaluate the function of YAP in glucose deprivation induced gene expression.
2023-11-29 | GSE215815 | GEO
Project description:In the analysis of a carbohydrate metabolite pathway, we found that a mutant strain of Corynebacterium glutamicum deficient in pfkB1, which encodes fructose-1-phosphate kinase, showed interesting characteristics. After aerobically cultivated with fructose as a carbon source, this mutant consumed glucose and produced lactate more than 2-fold as compared with the wild-type under conditions of oxygen deprivation. This considerably higher fermentation capacity was unique for the combination of the pfkB1 deletion and fructose cultivation. On the basis of the metabolome and transcriptome analyses, we identified marked intracellular accumulation of fructose-1-phosphate and significant upregulation of several genes related to the phosphoenolpyruvate:carbohydrate phosphotransferase system, glycolysis, and organic acid synthesis in this strain. Therefore, the considerably enhanced glucose consumption and organic acid production presumably resulted from a relief of transcriptional repression driven by global regulator SugR owing to the accumulated fructose-1-phosphate. Furthermore, we demonstrated that engineered strains overexpressing the above upregulated genes showed enhanced glucose consumption and organic acid production. The ppc deletion mutant of the engineered strain consumed 1,250 mM glucose and produced 2,390 mM lactate in 48 h under oxygen deprivation, which are 2.6- and 2.7-fold higher than the corresponding parameters of the ppc-deleted wild-type.
2016-11-28 | GSE83383 | GEO
Project description:Expression analysis of the glucose deprivation-induced human tumor cell responses
| PRJNA168162 | ENA
Project description:Erastin is a small molecular compound which inhibits the system Xc- and prevents the import of cystine, reducing glutathione (GSH) biosynthesis and glutathione peroxidase 4 (GPX4) activity, and finally inducing cell death via ferroptosis. To establish a model of Erastin induced ferroptosis in glioma cells, U87 cells were treated of Erastin (10 μM, 72 h). Combination analysis of HiChIP, ChIP-seq and RNA-seq data suggests that change of chromatin loops mediated by 3D chromatin structure regulate gene expressions in glioma ferroptosis. Genes that regulated by 3D chromatin structure include genes that were reported function in ferroptosis like MDM2 and TXRND1. We propose a new regulatory mechanism governing glioma cell ferroptosis by 3D chromatin structure.
2023-10-23 | GSE236253 | GEO
Project description:Sleep is an evolutionarily conserved physiological process implicated in the consolidation of learning and memory. In our study, sleep deprivation-induced cognitive deficits in zebrafish are mediated through reduction in glucose metabolism to the hexosamine biosynthetic pathway. Therefore, we perform the microarray to confirm glucose metabolic pathway- and nerve system-related genes expression using mRNA from brains of control, sleep-deprived and fear-conditioned zebrafish groups.
2019-03-14 | GSE128217 | GEO