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ABSTRACT: UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells

OTHER RELATED OMICS DATASETS IN: E-GEOD-22334E-GEOD-22336

PROVIDER: PRJNA127511 | ENA |

REPOSITORIES: ENA

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UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells

Project description:This SuperSeries is composed of the following subset Series: GSE22334: Induction of apoptotic processes in Capan-1 pancreatic carcinoma cells by restoration of p16INK4a expression GSE22336: UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells: GNE silencing Refer to individual Series

2010-08-01 | E-GEOD-22337 | biostudies-arrayexpress

Homo sapiens

Project description:UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells: GNE silencing

| PRJNA129245 | ENA

E-GEOD-22336

Project description:UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells: GNE silencing

2015-08-12 | E-GEOD-22336 | ExpressionAtlas

UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells: GNE silencing

Project description:Early invasive growth and metastasis are features of pancreatic cancer that rely on resistance to anoikis, an apoptosis program activated upon loss of adequate matrix anchorage. Re-expression of the tumor suppressor p16 reversed anoikis resistance of pancreatic cancer cells. This conversion to an anoikis-susceptible phenotype was found to be associated with a striking loss of GNE mRNA expression, prompting us to address the role of GNE in pancreatic cancer in more detail. GNE catalyzes a rate-limiting key step of the sialic acid biosynthesis and may have additional functions in the nucleus. Pancreatic cancer cells Capan-1. Three GNE-silencing samples and three control samples.

2010-08-01 | E-GEOD-22336 | biostudies-arrayexpress

Induction of apoptotic processes in Capan-1 pancreatic carcinoma cells by restoration of p16INK4a expression

2010-08-01 | E-GEOD-22334 | biostudies-arrayexpress

Homo sapiens

Project description:Induction of apoptotic processes in Capan-1 pancreatic carcinoma cells by restoration of p16INK4a expression

| PRJNA129243 | ENA

E-GEOD-22334

Project description:Induction of apoptotic processes in Capan-1 pancreatic carcinoma cells by restoration of p16INK4a expression

2015-08-12 | E-GEOD-22334 | ExpressionAtlas

Protein kinase A controls the hexosamine pathway by tuning feedback inhibition of GFAT-1

Project description:The hexosamine pathway (HP) is a key anabolic pathway whose product uridine 5’-diphospho-N-acetyl-D-glucosamine (UDP-GlcNAc) is an essential precursor for all glycosylation processes in mammals. It modulates the ER stress response, is implicated in cancer and diabetes, and HP activation extends lifespan in Caenorhabditis elegans. The highly conserved glutamine fructose-6-phosphate amidotransferase 1 (GFAT 1) is the first and rate-limiting HP enzyme. GFAT 1 activity is modulated through UDP-GlcNAc feedback inhibition and by kinase signaling, including Ser205 phosphorylation by protein kinase A (PKA). The consequence and molecular mechanism of GFAT 1 PKA phosphorylation, however, remains poorly understood. Here, we identify the GFAT 1 R203H substitution that elevates UDP-GlcNAc levels in C. elegans, leading to ER stress resistance. In human GFAT-1, the R203H substitution interfered with UDP-GlcNAc inhibition and with PKA-mediated Ser205 phosphorylation. Of note, Ser205 phosphorylation had two discernible effects: It lowered baseline GFAT 1 activity while abolishing UDP-GlcNAc feedback inhibition. Thus, GFAT-1 phosphorylation by PKA uncoupled the feedback loop of the HP and depending on UDP-GlcNAc availability, phosphorylation by PKA lowers or enhances GFAT 1 activity in vivo. Mechanistically, our data indicate that the relative positioning of the two GFAT 1 domains might be affected by phosphorylation and we propose a model how Ser205 phosphorylation modulates the activity and feedback inhibition of GFAT 1.

2020-07-23 | PXD020451 | Pride

Gene expression of SKOV3 cells after no treatment or treatment with 50 microM peracetylated GlcNAc or peracetylated 4-deoxy-GlcNAc for three days

Project description:Heparan sulfate (HS), a long linear polysaccharide, is implicated in various steps of tumorigenesis, including angiogenesis. We successfully interfered with HS biosynthesis using a peracetylated 4-deoxy analog of the HS constituent GlcNAc and studied the compoundM-bM-^@M-^Ys metabolic fate and its effect on angiogenesis. The 4-deoxy analog was activated intracellularly into UDP-4-deoxy-GlcNAc and HS expression was inhibited up to ~96% (IC50 = 16 M-BM-5M). HS chain size was reduced, without detectable incorporation of the 4-deoxy analog, likely due to reduced levels of UDP-GlcNAc and/or inhibition of glycosyltransferase activity. Comprehensive gene expression analysis revealed reduced expression of genes regulated by HS binding growth factors as FGF-2 and VEGF. Cellular binding and signaling of these angiogenic factors was inhibited. Micro-injection in zebrafish embryos strongly reduced HS biosynthesis, and angiogenesis was inhibited in both zebrafish and chicken model systems. All these data identify 4-deoxy-GlcNAc as a potent inhibitor of HS synthesis which hampers pro-angiogenic signaling and neo-vessel formation. 9 samples were analyzed: 3 biological replicates from untreated SKOV3 cells, 3 biological replicates from SKOV3 cells treated with peracetylated GlcNAc, 3 biological replicates from SKOV3 cells treated with peracetylated 4-deoxy-GlcNAc

2013-08-23 | E-GEOD-48284 | biostudies-arrayexpress

The pancreatic cancer stem cell marker CD44v6 affects transcription, translation and signaling: consequences on exosome composition and delivery II

Project description:The miRNA profile between different pancreatic adenocarcinoma cells (A818.4, Capan-1) and different colorectal carcinoma cells (SW948, HT-29). The impact of a knockdown (kd) of function-relevant cancer stem cell markers (CD44v6, Tspan8, CD151, claudin7) on the miRNA profile. The kd cell miRNA profiles were compared with the wt cell as well as between the different kd miRNA profiles.

2018-08-25 | GSE119032 | GEO

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