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Gene expression profiles for hyperglycemia induced tumors and mammary glands compared to those in euglycemia

ABSTRACT: Analysis of hyperglycemia-induced tumor progression at gene expression level. The hypothesis tested in the present study was that hyperglycemia contributes to tumor growth and metastasis. Results provide important information of the response of hyperglycemia, such as specific NRG1 pathways, HER2-3 pathways, NF-kB pathways and anti-apoptotic related genes, up- or down-regulated.

ORGANISM(S): Mus musculus

PROVIDER: GSE40361 | GEO | 2012/08/24

SECONDARY ACCESSION(S): PRJNA173694

REPOSITORIES: GEO

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Gene expression profiles for hyperglycemia induced tumors and mammary glands compared to those in euglycemia

Project description:Analysis of hyperglycemia-induced tumor progression at gene expression level. The hypothesis tested in the present study was that hyperglycemia contributes to tumor growth and metastasis. Results provide important information of the response of hyperglycemia, such as specific NRG1 pathways, HER2-3 pathways, NF-kB pathways and anti-apoptotic related genes, up- or down-regulated. Total RNA obtained from tumor tissues of 10-week-old PyMT/PANIC and PyMT mice as well as mammary glands of 10-week-old PANIC-ATTAC and WT mice.

2012-08-24 | E-GEOD-40361 | biostudies-arrayexpress

Identification of Nrg1 enhancer binding proteins

Project description:Hyperglycemia is a risk factor for breast cancer-related morbidity and mortality. Hyperglycemia induces Neuregulin 1 (Nrg1) overexpression in breast cancer, which subsequently promotes tumor progression. However, molecular mechanisms underlying hyperglycemia-induced Nrg1 overexpression remain poorly understood. Here, We used DNA-protein pull-down using Nrg1 enhancer sequence as bait followed by LC/MS and identified RBPJ as a key component of the Nrg1 enhanceosome. We show that hyperglycemia causes active histone modifications at the Nrg1 enhancer, forming enhanceosome complexes where RBPJ, P300, and SETD1A are recruited to upregulate Nrg1 expression.

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Identification of Nrg1 enhancer binding proteins

2023-01-29 | PXD038668 | Pride

Hyperglycemia induced microRNAs in endothelial dysfunction

Project description:Hyperglycemia is a hallmark in prediabetes and type 2 diabetes mellitus (T2DM) which increases risk of micro and macrovascular complications such as diabetic retinopathy, diabetic nephropathy (microvascular complications), and peripheral vascular disease, cerebrovascular disease and cardiovascular diseases (macrovascular complications). Endothelial cells are affected in both cases. In this study, we investigated the miRNA expression changes in HUVECs during different glucose treatment (5mM, 10mM, 25mM and 40mM glucose) at various time intervals (6, 12, 24 and 48hrs). The results of miRNA microarray showed there is a correlation between hyperglycemia induced endothelial dysfunction and miRNA expression. In silico prediction showed that the following pathways: Regulation of actin cytoskeleton, PI3K-Akt signaling pathway, Apoptosis, Neurotrophin signaling pathway, and Insulin signaling pathway, were dysregulated during hyperglycemia. Majority of the pathways are related to apoptosis. 10 miRNAs (miR-26a-5p, -26b-5p, 29b-3p, 29c-3p, 125b-1-3p, -130b-3p, - 140-5p, -221-3p, -192-5p, and -320a,) showed increased expression with increasing concentration of glucose treatment. miR-26a-5p, -29b-3p, - 140-5p, -221-3p, and -192-5p are involves in endothelial apoptosis. Our study revealed miRNAs (miR-29b-3p and – 192-5p) with known mRNA targets (BCL2 and MCL1) showed expression pattern inversely correlating with their respective target mRNAs. Therefore these miRNAs could involve in the endothelial dysfunction due to hyperglycemia.

2016-05-23 | GSE74296 | GEO

Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells (ChIP-seq)

Project description:We report that hyperglycemia-mediated induction of genes and pathways associated to endothelial dysfunction occur through modulation of acetylated H3K9/K14 inversely correlated with methyl-CpG content. Examination of H3K9/K14 histone acetylation and DNA methylation in hyperglycemic conditions.

2011-06-01 | E-GEOD-29251 | biostudies-arrayexpress

BK5.ATF3-induced mammary tumors compared to normal mammary glands

Project description:Transcriptional profiling of mammary tumors that occur in parous, BK5.ATF3 mice, compared to normal mammary tissue

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Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells (gene expression)

2011-07-19 | E-GEOD-30780 | biostudies-arrayexpress

Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells (gene expression)

2011-07-20 | GSE30780 | GEO

Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells (ChIP-seq)

2011-06-01 | GSE29251 | GEO

Chronic hyperglycemia impairs metabolic switching of human myotubes

Project description:Skeletal muscle of insulin resistant individuals is characterized by lower fasting lipid oxidation and reduced ability to switch between lipid and glucose oxidation. The purpose of the present study was to examine if impaired metabolic switching could be induced by chronic hyperglycemia. Human myotubes were treated with or without chronic hyperglycemia (HG) (20 mmol/l glucose for 4 days), and the metabolism of [14C]oleic acid (OA) and [14C]glucose was studied. Acute glucose (5mmol/l) suppressed OA oxidation by 50% in normoglycemic (NG) (5.5 mmol/l glucose) cells. Myotubes exposed to chronic hyperglycemia showed a significantly reduced OA uptake and oxidation to CO2, whereas acid-soluble metabolites were increased. Glucose suppressibility, the ability of acute glucose to suppress lipid oxidation, was significantly reduced to 21%, while adaptability, the capacity to increase lipid oxidation with increasing fatty acid availability, was unaffected. Glucose uptake and oxidation was significantly reduced by about 40%. Substrate oxidation in presence of mitochondrial uncouplers showed that net and maximal oxidative capacities were significantly reduced after hyperglycemia, and the concentration of ATP was reduced by 25%. However, none of the measured mitochondrial genes were downregulated nor was mitochondrial content. Microarray showed that no genes were significantly regulated by chronic hyperglycemia. Addition of chronic lactate reduced both glucose and OA oxidation to the same extent as hyperglycemia, and this effect was specific for lactate. In conclusions, chronic hyperglycemia reduced substrate oxidation in skeletal muscle cells and impaired the metabolic switching. The effect is most likely due to an induced mitochondrial dysfunction.

2009-12-24 | GSE19620 | GEO

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