Glucose deprivation induced gene expression
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ABSTRACT:
PROVIDER: PRJNA668528 | ENA |
REPOSITORIES: ENA
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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:To assess the effect of sleep deprivation on glucose metabolism and elucidate the mechanism, we established the mouse model wth C57BL/6J that is useful for the intervention on sleep deprivation associated diabetes and evaluate the liver metabolism and gene expression. Single six hours sleep deprivation induced increased hepatic glucose production assessed by pyruvate tolerance test and the hepatic triglyceride content was significantly higher in the sleep deprivation group than freely sleeping control group. Liver metabolites such as ketone bodies were increased in sleep deprivation group. Some gene expressions which associated with lipogenesis were increased.
2016-12-27 | GSE92913 | GEO
Project description:We investigated the function of the mTORC1 substrates and mRNA translation regulators 4EBP1/2 in the response to glucose deprivation. We uncovered that targeting 4EBP1/2 expression had a direct impact on the survival rates of cells challenged with glucose deprivation. To further define the mechanisms underlying 4EBP1/2 function under glucose deprivation, we conducted a proteomics analysis of HEK293 shRNA control and HEK293 shRNA 4EBP1/2 grown in basal media or under glucose deprivation (1 mM glucose containing media) for 30 hours.
2024-03-28 | PXD040931 | Pride
Project description:Glucose is the main substrates of cancer cell metabolism. Relying on glucose for rapid proliferation and maintaining intracellular redox homeostasis is one of the hallmarkers of cancer cells. During physiology or cancer treatment, cancer cells will face a limited supply of glucose. In these case, cancer cells will undergo cell death . The plasticity of cancer cells is the main factor that allows cancer cells to survive this difficult situation. So in order to better understand the cplasticity of cancer cells, we use glucose-free medium to treat the colorectal cancer cell line HCT116, and perform RNA-Seq analysis on the treated samples.
2021-05-01 | GSE159351 | GEO
Project description:Ischemia lead to neuronal injury. Dexmedetomidine and astrocytes are likely to protect neuronal cells against ischemia-induced injury. We used microarrays to examine the gene expression variation in astrocytes activated by oxygen-glucose deprivation and reoxygenation stress and identified distinct classes of genes up- and down-regulated by dexmedetomidine pretreatment.
2021-02-05 | GSE166193 | GEO
Project description:Migroglia cells were exposed to oxygen-glucose deprivation (OGD) for 3 h. The mRNA was isolated and the expression profiles of OGD-activated cells were compared with the profiles of resting cells.
2015-11-23 | GSE63505 | GEO
Project description:The tumor microenvironment is characterized by low glucose and hypoxia. It is well known that changes in the tumor microenvironment, such as hypoxia and low glucose, can increase the production of VEGF. Although the role of hypoxia in the regulation of VEGF production is well understood, the mechanism linking glucose deprivation (GD) to tumor growth and angiogenesis is unclear. Here, GD (a physiological stimulus) was used to treat human tumor cells. The transcriptional reprogramming of tumor cells by GD was measured with microarray technology to provide a comprehensive analysis of the gene expression profile underlying the GD treatment. Our study suggested that GD initiates an angiogenic switch by increasing the expression of proangiogenic mediators (VEGF, FGF2, IL6, etc.) and decreasing the expression of angiogenesis inhibitors (THBS1, CXCL14 and CXCL10). The markers of Unfolded Protein Response (UPR) (Grp78/Bip, CHOP, ATF4, etc.) were significantly increased. The above results suggest GD may regulate angiogenesis through activation of the UPR. UM-SCC-81B cells (human oral squamous cell carcinoma cell line) were treated with glucose deprivation (GD) for 4 hours (UM-SCC-81B-GD-4) and 24 hours (UM-SCC-81B-GD24). Cells without treatment were used as a non-treatment control (UM-SCC-81B-NT). Each sample was analyzed once, i.e., without biological replicates. The expression of the genes of interest was confirmed with real-time PCR, ELISA and Western blot.
2012-10-25 | E-GEOD-38583 | biostudies-arrayexpress
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:This microarray experiment was designed to identify genes and pathways modulated in glucose deprivation resistant (GDR) and glucose deprivation sensitive (GDS) clones of ovarian cancer xenografts. Tumors were established in NOD/SCID mice by s.c. injection of human ovarian cancer cells (IGROV-1 and SKOV3). After sacrifice GDR and GDS clones were obtained from ex vivo cultures of tumors. Once isolated, GDR and GDS clones were cultivated in normal-glucose (0h) or low-glucose condition (6 h and 24 h). Two different time points were selected to investigate both early (6 h) and late (24 h) transcriptional effects of glucose deprivation in IGROV-1 and SKOV3-derived clones. Total RNA was extracted from samples and hybridized on Affymetrix GeneChip™ PrimeView™ Human Gene Expression Arrays. Based on assessment of RNA quality and on quality control analyses (including MAplots and boxplots), only one sample, corresponding to GDR condition at 6 h of glucose deprivation in SKOV3 model, was excluded because it was deemed not suitable for data analysis. In order to evaluate the effects of glucose deprivation in the two models, expression data of IGROV-1 and SKOV3-derived GDR and GDS clones were normalized and analyzed separately. Raw microarray data and pre-processed data matrices are available together with the applied protocols. Results of differential expression analysis are provided as supplementary tables of the associated publication.
2023-05-31 | E-MTAB-12150 | biostudies-arrayexpress
Project description:The role of H2A monoubiquitination at K119 in regulating gene expression and cellular function upon glucose deprivation is unknown. Here, we conducted ChIP-seq for UMRC6 cells cultured with or without glucose for 8 hours using primary antibody against H2Aub. Genes with deregulated H2Aub level under glucose starvation condition were particular of interest.
2020-03-31 | GSE137885 | GEO