Metabolic control of glucose degradation in yeast and tumor cells

2006 ◽  
pp. 1-28 ◽  
Author(s):  
Armin Fiechter ◽  
Felix K. Gmünder
Keyword(s):  
Metabolic Control ◽  
Tumor Cells

scholarly journals Platelets in tumor metastasis: generation of adenosine diphosphate by tumor cells is specific but unrelated to metastatic potential

Blood ◽  
1988 ◽  
Vol 71 (4) ◽  
pp. 844-849 ◽  
Author(s):  
G Grignani ◽  
GA Jamieson
Keyword(s):  
Metabolic Control ◽  
Tumor Cells ◽  
Feedback Inhibition ◽  
Cell Damage ◽  
Membrane Damage ◽  
Adenosine Diphosphate ◽  
Metastatic Potential ◽  
Cell Number ◽  
Murine Melanoma ◽  
Culture Supernatants

Abstract Human 253J urinary carcinoma cells and the F1 (low-metastatic) and F10 (high-metastatic) variants of the B16 murine melanoma cell line have been shown to activate heparinized human platelets by an adenosine diphosphate (ADP)-dependent mechanism based on inhibition by creatine phosphate/creatine phosphokinase and the identification of aggregating concentrations (1 to 2 mumol/L) of ADP in cell-free culture supernatants by high-performance liquid chromatography. Aggregation did not occur in citrated samples, and hirudin was without effect. Studies were carried out to determine whether extracellular ADP arose from nonspecific cell damage during cell isolation and manipulation or was a specific process under control of the tumor cells themselves. Tumor cell damage during harvesting was shown not to be a factor because the amounts of ADP produced by the three cell lines (a) were inversely related to the appearance of lactic dehydrogenase in the culture supernatants and (b) were similar when measured in confluent monolayers, either in tumor cells after detachment and resuspension or after crossover studies involving culture in, alternatively, Hanks' balanced salt solution and minimal essential medium. Metabolic control of ADP production was indicated by the fact that (a) it was not dependent on cell number, which suggests feedback inhibition; (b) it was reduced 60% when tumor cells were treated with p- chloromercuribenzene sulfonate; and (c) it was completely abolished in those treated with iodoacetic acid, which might be expected to increase nonspecific leakage. These studies indicate that ADP production by these three lines does not arise due to leakage induced by nonspecific membrane damage during cell harvesting and manipulation but is a discrete process under metabolic control of the tumor cells. Moreover, in B16 murine melanoma cells the ability to produce ADP and to support platelet aggregation appears to be unrelated to metastatic potential insofar as identical results were obtained with the F1 and F10 variants.

scholarly journals Platelets in tumor metastasis: generation of adenosine diphosphate by tumor cells is specific but unrelated to metastatic potential

Blood ◽  
1988 ◽  
Vol 71 (4) ◽  
pp. 844-849
Author(s):  
G Grignani ◽  
GA Jamieson
Keyword(s):  
Metabolic Control ◽  
Tumor Cells ◽  
Feedback Inhibition ◽  
Cell Damage ◽  
Membrane Damage ◽  
Adenosine Diphosphate ◽  
Metastatic Potential ◽  
Cell Number ◽  
Murine Melanoma ◽  
Culture Supernatants

Human 253J urinary carcinoma cells and the F1 (low-metastatic) and F10 (high-metastatic) variants of the B16 murine melanoma cell line have been shown to activate heparinized human platelets by an adenosine diphosphate (ADP)-dependent mechanism based on inhibition by creatine phosphate/creatine phosphokinase and the identification of aggregating concentrations (1 to 2 mumol/L) of ADP in cell-free culture supernatants by high-performance liquid chromatography. Aggregation did not occur in citrated samples, and hirudin was without effect. Studies were carried out to determine whether extracellular ADP arose from nonspecific cell damage during cell isolation and manipulation or was a specific process under control of the tumor cells themselves. Tumor cell damage during harvesting was shown not to be a factor because the amounts of ADP produced by the three cell lines (a) were inversely related to the appearance of lactic dehydrogenase in the culture supernatants and (b) were similar when measured in confluent monolayers, either in tumor cells after detachment and resuspension or after crossover studies involving culture in, alternatively, Hanks' balanced salt solution and minimal essential medium. Metabolic control of ADP production was indicated by the fact that (a) it was not dependent on cell number, which suggests feedback inhibition; (b) it was reduced 60% when tumor cells were treated with p- chloromercuribenzene sulfonate; and (c) it was completely abolished in those treated with iodoacetic acid, which might be expected to increase nonspecific leakage. These studies indicate that ADP production by these three lines does not arise due to leakage induced by nonspecific membrane damage during cell harvesting and manipulation but is a discrete process under metabolic control of the tumor cells. Moreover, in B16 murine melanoma cells the ability to produce ADP and to support platelet aggregation appears to be unrelated to metastatic potential insofar as identical results were obtained with the F1 and F10 variants.

GENERATION OF ADP BY HUMAN AND MURINE TUMOR CELLS IS SPECIFIC BUT IS UNRELATED TO METASTATIC POTENTIAL

1987 ◽  
Author(s):  
G A Jamieson ◽  
G Grignani
Keyword(s):  
Tumor Cell ◽  
Metabolic Control ◽  
Tumor Cells ◽  
Cell Damage ◽  
Metastatic Potential ◽  
Iodoacetic Acid ◽  
Human Platelets ◽  
Significant Difference

The ability of tumor cells to activate platelets may facilitate the metastatic process. It has been generally assumed that the production of ADP by tumor cells is due to non-specific damage during harvesting in vitro or, in vivo, by frictional interactions with the capillary wall. The present work shows that tumor cell ADP arises not from cell damage but by a specific process under metabolic control. The human 253J urinary carcinoma cell line activated heparinized human platelets by an ADP-dependent mechanism based on inhibition by CP/CPK and the identification of aggregating concentrations (1 uM) of ADP in the cell-free supernatant by HPLC. Tumor cell damage during harvesting was shown not to be a factor since (i) the amount of ADP secreted was unrelated to the appearance of LDH, (ii) was similar when measured in confluent monolayers, in tumor cells after detachment and resuspension or following crossover studied in HBSS and MEM, and (iii) was constant at varying tumor cell concentrations. Metabolic control of ADP generation or transport was indicated by the fact that it was reduced 50 in tumor cells treated with p-chloromercuribenzene sulfonate and was completely abolished in those treated with iodoacetic acid. In order to determine whether this metabolically controlled generation of ADP was related to metastatic potential, we carried out identical experiments with the FI (low) and F10 (high) metastatic variants of the Bl6 murine melanoma line. The amounts of ADP produced by the B16 cells were about twice as great as with the human 253J cells but there was no significant difference between the amounts of ADP generated by FI and F10 variants. These studies demonstrate that ADP production by tumor cells is a discrete process under metabolic control but is not directly related to the metastatic potential of individual tumor cell lines.

Application of metabolic-control logic to fuel utilization and its significance in tumor cells

1991 ◽  
Vol 31 ◽  
pp. 225-246 ◽  
Author(s):  
Eric A. Newsholme ◽  
Mary Board
Keyword(s):  
Metabolic Control ◽  
Tumor Cells ◽  
Fuel Utilization ◽  
Control Logic

scholarly journals Complex N-Glycan and Metabolic Control in Tumor Cells

2007 ◽  
Vol 67 (20) ◽  
pp. 9771-9780 ◽  
Author(s):  
Richard Mendelsohn ◽  
Pam Cheung ◽  
Lloyd Berger ◽  
Emily Partridge ◽  
Ken Lau ◽  
...  
Keyword(s):  
Metabolic Control ◽  
Tumor Cells

Membranous alterations in the cytoplasm and nucleus in a primitive neuroectodermal tumor of the brain

1978 ◽  
Vol 36 (2) ◽  
pp. 628-629
Author(s):  
C. N. Sun ◽  
C. Araoz ◽  
H. J. White
Keyword(s):  
Nuclear Envelope ◽  
Tumor Cells ◽  
Osmium Tetroxide ◽  
Primitive Neuroectodermal Tumor ◽  
Uranyl Acetate ◽  
Neuroectodermal Tumor ◽  
Annulate Lamellae ◽  
Lead Citrate ◽  
Thin Sections ◽  
The Brain

The ultrastructure of a cerebral primitive neuroectodermal tumor has been reported previously. In the present case, we will present some unusual previously unreported membranous structures and alterations in the cytoplasm and nucleus of the tumor cells.Specimens were cut into small pieces about 1 mm3 and immediately fixed in 4% glutaraldehyde in phosphate buffer for two hours, then post-fixed in 1% buffered osmium tetroxide for one hour. After dehydration, tissues were embedded in Epon 812. Thin sections were stained with uranyl acetate and lead citrate.In the cytoplasm of the tumor cells, we found paired cisternae (Fig. 1) and annulate lamellae (Fig. 2) noting that the annulate lamellae were sometimes associated with the outer nuclear envelope (Fig. 3). These membranous structures have been reported in other tumor cells. In our case, mitochondrial to nuclear envelope fusions were often noted (Fig. 4). Although this phenomenon was reported in an oncocytoma, their frequency in the present study is quite striking.

Ulcerogenic Tumors of the Pancreas

1968 ◽  
Vol 26 ◽  
pp. 186-187
Author(s):  
J. C. Garancis ◽  
J. F. Kuzma ◽  
S. D. Wilson ◽  
E. H. Ellison
Keyword(s):  
Endoplasmic Reticulum ◽  
Tumor Cells ◽  
Islet Cell ◽  
Disease Process ◽  
Central Core ◽  
Islet Cell Tumors ◽  
Opaque Zone ◽  
Granular Form ◽  
Zollinger Ellison Syndrome

It has been proposed that a gastrin-like hormone elaborated by non-beta islet tumors of the pancreas may be responsible for a fulminating ulcer diathesis. Subsequently, a potent gastric secretagogue was isolated from ulcerogenic tumors of the pancreas. This disease process is known now as “Zollinger-Ellison syndrome”.In our studies of two cases of Zollinger-Ellison syndrome, pancreatic lesions were identified as alpha islet cell tumors (Fig. 1). Tumor cells were fairly uniform. The sizes of the alpha granules were not significantly different, but their number and distribution varied greatly from one cell to another. Each granule consisted of a round, highly dense central core, separated from the limiting membrane by an opaque zone. The granular form of the endoplasmic reticulum was particularly prominent. Numerous mitochondria, round or elongated, were dispersed throughout the cytoplasm. Individual or clusters of lysosomes were observed in the majority of cells.

Glucose metabolism in cancer cells: immunogold localization of hexokinase to the outer mitochondrial membrane

1995 ◽  
Vol 53 ◽  
pp. 1044-1045
Author(s):  
Krishan K. Arora ◽  
Glenn L. Decker ◽  
Peter L. Pedersen
Keyword(s):  
Tumor Cells ◽  
Mitochondrial Membrane ◽  
Present Report ◽  
Large Fraction ◽  
Mitochondrial Fraction ◽  
Immunogold Labeling ◽  
Outer Mitochondrial Membrane ◽  
Immunogold Localization ◽  
Hexokinase Activity ◽  
Normal Tissues

Hexokinase (ATP: D-hexose 6-phophotransferase EC 2.7.1.1) is the first enzyme of the glycolytic pathway which commits glucose to catabolism by catalyzing the phosphorylation of glucose with ATP. Previous studies have shown diat hexokinase activity is markedly elevated in rapidly growing tumor cells exhibiting high glucose catabolic rates. A large fraction (50-80%) of this enzyme activity is bound to the mitochondrial fraction (1,2) where it has preferred access to ATP (3). In contrast,the hexokinase activity of normal tissues is quite low, with one exception being brain which is a glucose-utilizing tissue (4). Biochemical evidence involving rigorous subfractionation studies have revealed striking differences between the subcellular distribution of hexokinase in normal and tumor cells [See review by Arora et al (4)].In the present report, we have utilized immunogold labeling techniques to evaluate die subcellular localization of hexokinase in highly glycolytic AS-30D hepatoma cells and in the tissue of its origin, i.e., rat liver.

Sequential detection of mRNA for the chemokine IL-8 and macrophages (F4/80) in human melanoma

1995 ◽  
Vol 53 ◽  
pp. 1008-1009
Author(s):  
C.D. Bucana ◽  
R. Sanchez ◽  
R. Singh ◽  
I.J. Fidler
Keyword(s):  
Tumor Cells ◽  
Nude Mice ◽  
Constitutive Expression ◽  
Metastatic Potential ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Angiogenic Factor ◽  
Infiltrating Cells ◽  
Immunoperoxidase Assay ◽  
Multifunctional Cytokine

The purpose of this study was to demonstrate by ISH the presence of IL-8 mRNA, and by immunohistochemistry (IHC) the presence of the chemokine IL-8 and the distribution of infiltrating macrophages in subcutaneous melanomas in the same tumor. IL-8 is a multifunctional cytokine produced by melanoma cells, activated macrophages and monocytes and it has been shown to be a growth and angiogenic factor for tumor cells. More recently it was shown that constitutive expression of IL-8 correlated directly with metastatic potential of human melanoma cells in nude mice. IL-8 content of a solid tumor as determined by Western blot analysis does not take into account the contribution of macrophages. Previous studies showed that murine tumors contain many infiltrating cells interspersed among tumor cells whereas human tumors growing in nude mice exhibit macrophages at the periphery or between tumor islands. In this study we demonstrate the expression of IL-8 and the distribution of macrophages by immunoperoxidase assay and IL-8 mRNA by ISH.

Temporal and spatial interrelationships of confronting cisternae to nuclear envelope

1992 ◽  
Vol 50 (1) ◽  
pp. 930-931
Author(s):  
John R. Palisano
Keyword(s):  
Endoplasmic Reticulum ◽  
Nuclear Envelope ◽  
Tumor Cells ◽  
Hela Cells ◽  
Microscopic Investigation ◽  
Electron Microscopic Investigation ◽  
Serial Sections ◽  
Electron Microscopic ◽  
Fetal Rat ◽  
Temporal And Spatial

Although confronting cistemae (CC) have been observed in a variety of tumor cells and normal fetal rat, mouse, and human epithelial tissues, little is known about their origin or role in mitotic cells. While several investigators have suggested that CC arise from nuclear envelope (NE) folding back on itself during prophase, others have suggested that CC arise when fragments of NE pair with endoplasmic reticulum. An electron microscopic investigation of 0.25 um thick serial sections was undertaken to examine the origin of CC in HeLa cells.

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