Sugar Composition of Mammalian Cell Surface Membrane: A Function of Carbon Source

Paolini, Domenic; Humphrey, L.P.; Gonzalez, Federico; Colofiore, Joseph; Rossow, Peter W.; Amos, Harold

doi:10.1016/b978-0-12-326150-2.50016-x

Cited by 5 publications

(5 citation statements)

References 26 publications

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“…The data extend the observations of others who demonstrated that using alternative carbon sources in media can lead to changes in cell size and morphology (8,9,26). It has been reported previously that substituting other sugars for glucose in cell culture media may influence cell differentiation, sugar nucleotide pools, and gene expression (26–28).…”

Section: Discussionsupporting

confidence: 89%

“…It has been reported previously that substituting other sugars for glucose in cell culture media may influence cell differentiation, sugar nucleotide pools, and gene expression (26–28). Although it seemed likely that the addition of fructose might modify the expression of genes controlling cell surface glycomic phenotype, none were observed in our microarray studies (data not shown).…”

Section: Discussionmentioning

confidence: 99%

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Fructose as a carbon source induces an aggressive phenotype in MDA-MB-468 breast tumor cells

Monzavi‐Karbassi

Hine²,

Stanley³

et al. 2010

Int J Oncol

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Aberrant glycosylation is a universal feature of cancer cells, and certain glycan structures are well-known markers for tumor progression. Availability and composition of sugars in the microenvironment may affect cell glycosylation. Recent studies of human breast tumor cell lines indicate their ability to take up and utilize fructose. Here we tested the hypothesis that adding fructose to culture as a carbon source induces phenotypic changes in cultured human breast tumor cells that are associated with metastatic disease. MDA-MB-468 cells were adapted to culture media in which fructose was substituted for glucose. Changes in cell surface glycan structures, expression of genes related to glycan assembly, cytoskeleton F-actin, migration, adhesion and invasion were determined. Cells cultured in fructose expressed distinct cell-surface glycans. The addition of fructose affected sialylation and fucosylation patterns. Fructose feeding also increased binding of leukoagglutinating Phaseolus vulgaris isolectin, suggesting a possible rise in expression of branching β-1, 6 GlcNAc structures. Rhodamine-phalloidin staining revealed an altered F-actin cytoskeletal system. Fructose accelerated cellular migration and increased invasion. These data suggest that changing the carbon source of the less aggressive MDA-MB-468 cell line induced characteristics associated with more aggressive phenotypes. These data could be of fundamental importance due to the markedly increased consumption of sweeteners containing free fructose in recent years, as they suggest that the presence of fructose in nutritional micro-environment of tumor cells may negatively affect the outcome for some breast cancer patients.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Fructose as a carbon source induces an aggressive phenotype in MDA-MB-468 breast tumor cells

Monzavi‐Karbassi

Hine²,

Stanley³

et al. 2010

Int J Oncol

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“…highly speculative with our current state of knowledge. However, in view of the findings that changes in the pools of nucleotide sugars are associated with modifications of glycosylation of membrane proteins (Paolini et al, 1978;Morin et al, 1983), further studies should investigate whether the dedifferentiation of Glc+ HT-29 cells could be associated with some particular changes in the pools of sugar nucleotides, and also of other intermediates of glucose metabolism, as compared to differentiated Glc ~ cells.…”

Section: -mentioning

confidence: 99%

Enterocytic differentiation of a subpopulation of the human colon tumor cell line HT‐29 selected for growth in sugar‐free medium and its inhibition by glucose

Zweibaum

Pinto

Chevalier

et al. 1985

Journal Cellular Physiology

313

193

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In order to study the effect of glucose on the differentiation of cultured human colon cancer cells, a subpopulation of HT-29 cells was selected for its capacity to grow in the total absence of sugar. These cells (Glc-cells) exhibit, after confluency, an enterocytic differentiation, in contrast to cells grown with glucose (Glc+ cells), which always remain undifferentiated. The differentiation is characterized by a polarization of the cell layer with apical brush borders and tight junctions, and by the presence of sucrase-isomaltase. The differentiation of Glc- cells is reversible: the addition of glucose to postconfluent cultures of Glc- cells results in an inhibiting effect on the expression of sucrase-isomaltase; switching growing cultures of Glc- cells to the Glc+ medium for several passages results in a progressive reversion to the undifferentiated state, which is completed after seven passages. The dedifferentiation process is associated with a parallel, passage-related, increase in the rates of glucose consumption and lactic acid production, and decreases of intracellular glycogen content, which return to the values of the undifferentiated original Glc+ cells. The values of these metabolic parameters are correlated, at each passage, with the degree of dedifferentiation of the cells. When these dedifferentiated cells, after having been cultured in Glc+ medium for 20 passages, are switched back to the Glc- medium, they readily grow without mortality, and reexpress the same enterocytic differentiation as the parent Glc- cells. These results show that the capacity of this subpopulation to grow and differentiate in the absence of sugar is a stable characteristic. They further suggest that glucose metabolism interferes with the program of differentiation of HT-29 cells.

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“…In experiments in which naturally occurring monosaccharides were substituted (5.5 mM) for glucose in the growth medium, Amos and his colleagues found that not only the structure of the cell was altered (18) but also the monosaccharide composition ofthe membrane (19). The growth conditions for these experiments were different from those reported here; we maintained glucose in the medium as the major carbon source and added other sugars.…”

Section: Resultsmentioning

confidence: 51%

Specific monosaccharide inhibition of active sodium channels in neuroblastoma cells.

Giovanni¹,

Kessel²,

Glick³

1981

Proc. Natl. Acad. Sci. U.S.A.

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L-Fucose and D-galactose in low concentrations (0.27 or 2.7 mM) inhibited the induction of active Na+ channels in mouse and-human neuroblastoma cells when the monosaccharides were added to the culture medium for 4 days with the inducing agent dimethyl sulfoxide. Active Na+ ionophores were determined by measurement of the toxin-stimulated efflux of 'Rb from the cells. At the same time, the amount of a radioactive glycoprotein (Mr 200,000), which was shown previously to be associated with neurite and. membrane preparations from cells with active Na+ channels, was decreased. Cell growth and viability were not affected. The nonphysiological isomer D-fucose or the addition of D-glucose in the same concentration did not inhibit differentiation. Vibriocholerae neuraminidase, added to the cells prior to the stimulation of "Rb efflux by veratridine and scorpion venom, was inhibitory. The implications of these findings, which suggest a key role for glycoproteins in at least a portion of the excitability process, are discussed.

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Sugar Composition of Mammalian Cell Surface Membrane: A Function of Carbon Source

Cited by 5 publications

References 26 publications

Fructose as a carbon source induces an aggressive phenotype in MDA-MB-468 breast tumor cells

Fructose as a carbon source induces an aggressive phenotype in MDA-MB-468 breast tumor cells

Enterocytic differentiation of a subpopulation of the human colon tumor cell line HT‐29 selected for growth in sugar‐free medium and its inhibition by glucose

Specific monosaccharide inhibition of active sodium channels in neuroblastoma cells.

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