RNA changes upon glucose starvation
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE252314 | GEO | 2025/01/01
REPOSITORIES: GEO
Similar Datasets
Project description:This data set consists of a long term glucose starvation time course of E. coli grown in minimal media for up to two weeks. Unlike previous studies of long term starvation,Our study focuses on the physiological response of E. Coli in stationary phase as a result of being starved for glucose, not on the genetic adaptation of E. coli to utilize alternative nutrients.
2015-08-24 | PXD002140 | Pride
Project description:Adaptation of Lactococcus lactis towards progressive carbon starvation is mediated by three different types of transcriptomic responses: i) global responses, i.e. general decrease of functions linked to bacterial growth and lack of induction of the general stress response, ii) specific responses functionally related to glucose exhaustion, i.e. under expression of central metabolism genes, induction of alternative sugars transport and metabolism genes, induction of arginine deiminase pathway genes and iii) other responses never described previously during carbon starvation. Keywords: stress response, time course
2008-02-23 | GSE5761 | GEO
Project description:RNA changes upon glucose starvation
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Project description:The hypothalamic-pituitary-adrenal (HPA) axis forms a complex neuroendocrine system that interacts directly via feedforward and feedback reactions to regulate the body’s response to stress such as starvation. In contrast with the glucocorticoid receptor (GR), ZBTB32 (zinc finger and BTB domain containing 32) is a transcription factor with very poorly described functional relevance in physiology. We investigated the importance of ZBTB32 on the HPA axis functioning and found that it is essential for the production of glucocorticoids (GCs) in response to starvation, because ZBTB32-/- mice fail to increase the GC production during prolonged absence of nutrients. In terms of mechanism, GR-mediated upregulation of adrenal Scarb1 gene expression was absent in ZBTB32-/- mice, implicating defective cholesterol import as the cause of the poor GC synthesis. Lower GC levels in ZBTB32-/- mice are further associated with aberrations in the metabolic adaptation to starvation, which could potentially explain the progressive weight gain of ZBTB32-/- mice. Moreover, this study identifies that ZBTB32 performs a crosstalk with the GR in the metabolic adaptation to starvation via regulation of adrenal GC production.
2021-06-08 | GSE176277 | GEO
Project description:Tumor chemoresistance is often associated to high aerobic glycolysis rates and reduced oxidative phosphorylation by cancer cells, a phenomenon called the “Warburg effect”. Thus, a treatment reversing the Warburg effect could decrease tumor cell survival both in the presence or absence of chemotherapy. Short-term starvation (STS) could accomplish this task since it is accompanied by a glucose and amino acid decrease and fatty acid increase, which require respiration for energy production. We tested the cytotoxicity of STS+Oxaliplatin on colon cancer cells by Trypan Blue, Carboxyfluorescein Succinimidyl ester and Annexin V staining. Reactive oxygen species production was measured by 2',7'-dichlorodihydrofluorescein diacetate staining. In vitro glucose consumption was evaluated by 18F-Fluoro-deoxyglucose uptake. Gene expression was tested by microarray analysis. Protein expression and activity were studied by western blot, proteomic analyses and spectrophotometric assays. CT26 bearing mice consumed only water for 48 hours (STS) before oxaliplatin treatment. Dynamic micro-Positron Emission Tomography and tumor growth measurements were performed. STS+Oxaliplatin cause a potent suppression of colon carcinoma growth and glucose consumption in in vitro and in vivo models. In CT26 cells, STS down-regulates aerobic glycolysis, and glutaminolysis, while increasing oxidative phosphorylation. STS-dependent increase in O2 consumption is associated with reduced ATP synthesis and increased oxidation. In combination with chemotherapy, these effects of STS cause additive toxicity to cancer cells. Our findings indicate that during and following STS the decreased glucose levels promote an anti-Warburg effect characterized by increased oxygen consumption but failure to generate ATP, resulting in oxidative damage and apoptosis. The experiment comprised for conditions: Control, Starvation, Oxaliplatin, and Starvation plus Oxaliplatin
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Project description:Proteome data obtained with timsTOF Pro of the fission yeast cells exposed to glucose starvation at four time points 0 (glucose rich conditions), 15, 60 and 120 minutes
2023-07-01 | MSV000092327 | MassIVE
Project description:TFE3-SLC36A1 axis promotes resistance to glucose starvation in kidney cancer cells
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Project description:"Starving cancer to death" is pursued for cancer therapy. An intriguing regime is to inhibit glucose transporter GLUT1 in cancer cells. But past attempts are challenged by that cancer cells can somehow tolerate starvation. In addition, during cancer progression, cancer cells may suffer from insufficient nutrient supply, for example due to insufficient angiogenesis. So uncovering mechanism of starvation resistance shall not only shed insight into cancer progression but also benefit cancer therapy. TFE3 is known as a transcription factor capable of activating autophagic genes. Physiological TFE3 activity is regulated by phosphorylation-triggered translocation, which is sensitive to nutrient status. We recently reported TFE3 constitutively localizes to cell nucleus in kidney cancer, promoting cell proliferation even under replete condition. But whether and how TFE3 affects kidney cancer cell sensitivity to starvation is unclear. In this study, we find TFE3 promotes kidney cancer cell resistance to glucose starvation. We show starvation triggers TFE3 protein stabilization through increasing its O-GlcNAcylation. Furthermore, through unbiased functional genomic study, we identify genes sensitive to TFE3 protein level, including SLC36A1, a lysosomal amino acid transporter. We find SLC36A1 is overexpressed in kidney cancer, promotes mTOR activity and kidney cancer cell proliferation. Importantly, SLC36A1 level is directly upregulated by TFE3 upon starvation, which enhances cellular resistance to starvation. Suppressing TFE3 or SLC36A1 significantly increased cellular sensitivity to GLUT1 inhibitor in kidney cancers. Collectively, we uncover a TFE3-SLC36A1 axis that responds to starvation and enhances starvation tolerance in kidney cancer.
2024-03-29 | GSE246789 | GEO
Project description:"Starving cancer to death" is pursued for cancer therapy. An intriguing regime is to inhibit glucose transporter GLUT1 in cancer cells. But past attempts are challenged by that cancer cells can somehow tolerate starvation. In addition, during cancer progression, cancer cells may suffer from insufficient nutrient supply, for example due to insufficient angiogenesis. So uncovering mechanism of starvation resistance shall not only shed insight into cancer progression but also benefit cancer therapy. TFE3 is known as a transcription factor capable of activating autophagic genes. Physiological TFE3 activity is regulated by phosphorylation-triggered translocation, which is sensitive to nutrient status. We recently reported TFE3 constitutively localizes to cell nucleus in kidney cancer, promoting cell proliferation even under replete condition. But whether and how TFE3 affects kidney cancer cell sensitivity to starvation is unclear. In this study, we find TFE3 promotes kidney cancer cell resistance to glucose starvation. We show starvation triggers TFE3 protein stabilization through increasing its O-GlcNAcylation. Furthermore, through unbiased functional genomic study, we identify genes sensitive to TFE3 protein level, including SLC36A1, a lysosomal amino acid transporter. We find SLC36A1 is overexpressed in kidney cancer, promotes mTOR activity and kidney cancer cell proliferation. Importantly, SLC36A1 level is directly upregulated by TFE3 upon starvation, which enhances cellular resistance to starvation. Suppressing TFE3 or SLC36A1 significantly increased cellular sensitivity to GLUT1 inhibitor in kidney cancers. Collectively, we uncover a TFE3-SLC36A1 axis that responds to starvation and enhances starvation tolerance in kidney cancer.
2024-03-29 | GSE246788 | GEO
Project description:We investigated eisosome rearrangement during glucose starvation. Pil1 phosphorylation was assessed in control and starvation conditions.
2020-03-23 | PXD017502 | Pride