Activity of glycogen depolymerizing enzymes in extracts from brain tumor tissue (anaplastic astrocytoma and glioblastoma multiforme).

Kotoński, B; Wilczek, Joanna; Madej, Janusz A.; Zarzycki, A; Hutny, Jan

doi:10.18388/abp.2001_3869

Cited by 5 publications

(1 citation statement)

References 10 publications

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“…By contrast, in brain tumor tissues (astrocytoma and glioblastoma) the activity of GP was found to be practically zero. Interestingly, glycogen present in detectable amounts in these tumors is hydrolytically degraded by upregulated α‐1,4‐glucosidases [207]. The physiological role of BGP is not well understood, but it seems to be involved in the induction of an emergency glucose supply during stressful periods such as anoxia and hypoglycaemia.…”

Section: Tumor‐specific Expression and Regulation Of Enzymes Involvedmentioning

confidence: 99%

Enzymatic features of the glucose metabolism in tumor cells

et al. 2011

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Glucose metabolism in tumor cellsan overviewGlucose is a treasured metabolic substrate for all human cells and is utilized for numerous metabolic functions (Fig. 1).1 Formation and degradation of glycogen serves as a means of internal glucose buffering. 2 The synthesis of ribose phosphates along the oxidative (OPPPW) and non-oxidative pentose phosphate pathway (NOPPPW) is essential for the synthesis of Many tumor types exhibit an impaired Pasteur effect, i.e. despite the presence of oxygen, glucose is consumed at an extraordinarily high rate compared with the tissue from which they originate -the so-called 'Warburg effect'. Glucose has to serve as the source for a diverse array of cellular functions, including energy production, synthesis of nucleotides and lipids, membrane synthesis and generation of redox equivalents for antioxidative defense. Tumor cells acquire specific enzyme-regulatory mechanisms to direct the main flux of glucose carbons to those pathways most urgently required under challenging external conditions such as varying substrate availability, presence of anti-cancer drugs or different phases of the cell cycle. In this review we summarize the currently available information on tumor-specific expression, activity and kinetic properties of enzymes involved in the main pathways of glucose metabolism with due regard to the explanation of the regulatory basis and physiological significance of the Warburg effect. We conclude that, besides the expression level of the metabolic enzymes involved in the glucose metabolism of tumor cells, the unique tumor-specific pattern of isozymes and accompanying changes in the metabolic regulation below the translation level enable tumor cells to drain selfishly the blood glucose pool that non-transformed cells use as sparingly as possible.Abbreviations ALD, aldolase; AMF, autocrine motility factor; BGP, brain-type glycogen phosphorylase; DHAP, dihydroxyacetone phosphate; EN, enolase; FASN, fatty acid synthetase; FH, fumarate hydratase; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GDPH, a-glycerophosphate dehydrogenase; GLUT, glucose transporter; GP, glycogen phosphorylase; G6PD, glucose 6-phosphate dehydrogenase; GPI, glucose 6-phosphate isomerase; 2HG, 2-hydroxyglutarate; HIF-1, hypoxia-inducible transcription factor; HK, hexokinase; IDH, isocitrate dehydrogenase; aKG, a-ketoglutarate; LDH, lactate dehydrogenase; MCT, monocarboxylate transporters; MPT, mitochondrial pyruvate transporter; NOPPPW, non-oxidative pentose phosphate pathway; OPPPW, oxidative pentose phosphate pathway; OXPHOS, oxidative phosphorylation; PDH, pyruvate dehydrogenase; PDHK-1, pyruvate dehydrogenase kinase; PFK-1, phosphofructokinase-1; PFK-2, phosphofructokinase-2; PFKFB, fructose 2,6-bisphosphatase; 6PGD, 6-phosphogluconate dehydrogenase; PGK, phosphoglycerate kinase; PGM, phosphoglycerate mutase; PHD, prolyl hydroxylase; PK, pyruvate kinase; PRPPS, phosphoribosyl pyrophosphate synthetase; ROS, reactive oxygen species; SDH, succhinate dehydrogenase; SMCT1, Na + -coupled lactate transpor...

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Section: Tumor‐specific Expression and Regulation Of Enzymes Involvedmentioning

confidence: 99%

Enzymatic features of the glucose metabolism in tumor cells

et al. 2011

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Influence of Ki‐ras‐driven oncogenic transformation on the protein network of murine fibroblasts

et al. 2007

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Ki-ras gene mutations that specifically occur in codons 12, 13 and 61 are involved in the carcinogenesis of acute myeloid leukemia, melanoma and different carcinomas. In order to define potential mutation-specific therapeutic targets, stable transfectants of NIH3T3 cells carrying different Ki-ras4B gene mutations were generated. Wild type Ki-ras transformants, mock transfectants and parental cells served as controls. These in vitro model systems were systematically analyzed for their protein expression pattern using two-dimensional gel electrophoresis followed by mass spectrometry and/or protein sequencing. Using this approach, a number of target molecules that are differentially but coordinately expressed in the ras transfectants were identified next to other proteins that exhibit a distinct regulation pattern in the different cell lines analyzed. The differentially expressed proteins predominantly belong to the families of cytoskeletal proteins, heat shock proteins, annexins, metabolic enzymes and oxidoreductases. Their validation was assessed by real-time quantitative RT-PCR and/or Western blot analysis. Our results suggest that the Ki-ras-transformed cells represent a powerful tool to study Ki-ras gene mutation-driven protein expression profiles. In addition, this approach allows the discovery of ras-associated cellular mechanisms, which might lead to the identification of physiological targets for pharmacological interventions of the treatment of Ki-ras-associated human tumors.

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Modulation of Carbohydrate Metabolism During N-Methyl N-Nitrosourea Induced Neurotoxicity in Mice: Role of Curcumin

Singla

Dhawan

2010

Neurochem Res

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The present study was carried out to elucidate the effectiveness of curcumin in mitigating the adverse effects caused by N-Methyl N-Nitrosourea (MNU) on mouse cerebellum and cerebrum. Male laca mice received either intravenous MNU treatment at a dose of 10 mg/kg bw in sterile double distilled water, curcumin alone 60 mg/kg bw in drinking water, or combined MNU and curcumin treatment on alternate days for a period of 2 months. The effects of different treatments were studied on carbohydrate metabolizing enzymes viz: hexokinase, glucose-6-phosphatase (G6P), glucose-6-isomerase (G6I), lactate dehydrogenase (LDH), succinate dehydrogenase (SDH) and glycogen levels. Curcumin supplementation to MNU treated mice was able to reduce significantly the activities of the G6P, G6I, hexokinase, LDH, SDH and increased the glycogen contents in both the regions of brain which were altered following MNU treatment. Hence, curcumin shall prove to be effective in ameliorating the adverse effects caused by MNU.

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Activity of glycogen depolymerizing enzymes in extracts from brain tumor tissue (anaplastic astrocytoma and glioblastoma multiforme).

Cited by 5 publications

References 10 publications

Enzymatic features of the glucose metabolism in tumor cells

Enzymatic features of the glucose metabolism in tumor cells

Influence of Ki‐ras‐driven oncogenic transformation on the protein network of murine fibroblasts

Modulation of Carbohydrate Metabolism During N-Methyl N-Nitrosourea Induced Neurotoxicity in Mice: Role of Curcumin

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