Contribution of α-d-galactopyranosyl end groups to attachment of highly and low metastatic murine fibrosarcoma cells to various substrates

Grimstad, Ivar Amund; Varani, James; McCoy, J. Philip

doi:10.1016/0014-4827(84)90195-2

Cited by 25 publications

(9 citation statements)

References 22 publications

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“…Others have noted major differences between metastatic cell lines using lectins with a specificity for GalNAc (Altevogt et al, 1983;Fogel et al, 1983;Kahn and Baumal, 1985). Blockage or removal of cell surface galactose residues has been shown to alter tumor cell attachment to basement membrane components in another tumor cell system (Grimstad et al, 1984). Although we did not detect inhibition of tumor-cell attachment with a-MeGal, the ability of GalNAc to inhibit tumor cell attachment to endothelial cells in the present study may be related to the adhesion of tumor cells to basement membrane components synthesized by endothelial cells.…”

Section: Tumor-cell Attachment To Vascular Endothelial Cellscontrasting

confidence: 72%

The role of tumor‐cell surface carbohydrate in experimental metastasis

Stanford

Starkey

Magnuson

1986

Intl Journal of Cancer

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Quantitative studies on the binding of concanavalin A (Con A) and wheat-germ agglutinin (WGA) to a series of rat hepatocarcinoma metastatic variants revealed a positive correlation between the amount of cell-surface-bound lectin and lung colonization potential. Scatchard analysis of Con A and WGA binding to 10 individual clones isolated from a subcutaneous (s.c.) tumor transplant and to tumor-cell isolates from 10 individual spontaneous lung metastases from the same animal showed diverse binding characteristics for these cell populations. Nevertheless, the expression of Con A receptor sites accurately predicted the lung colonization potential of 3 isolates from the lung metastases. Higher lectin binding curves were observed for the clones from the subcutaneous tumor than for the isolates from lung metastases. These data suggest that a high Con-A binding potential is indicative of a high lung colonization potential for these hepatocarcinoma cells, but that this phenotype may be rapidly lost during tumor outgrowth in the lungs. The binding of tumor cells to vascular endothelial cell monolayers was inhibited in the presence of Con A; however, no inhibition was observed with 2 other lectins. Attachment of tumor cells to endothelial cell monolayers was also inhibited by the monosaccharides methyl alpha-D-mannopyranoside and N-acetyl-D-galactosamine. Other monosaccharides tested did not alter the attachment of tumor cells to endothelial cell monolayers.

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Section: Tumor-cell Attachment To Vascular Endothelial Cellscontrasting

confidence: 72%

The role of tumor‐cell surface carbohydrate in experimental metastasis

Stanford

Starkey

Magnuson

1986

Intl Journal of Cancer

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“…Lectin-resistant mutant cell lines often possess altered adhesive properties (6,30,31), and some specificity in the ability of cellular glycopeptides to inhibit adhesion to extracellular matrix molecules has been demonstrated (32). Treatment of cells with either glycosidases (33), lectins (33), tunicamycin (34,35), or neuraminidase (31) modulates their attachment and spreading in vitro. Recently, cell-surface lectins on normal hepatocytes that aggregate liver-metastasizing tumor cells and that may be involved in the organ selectivity of these cells have been identified (36)(37)(38).…”

Section: Discussionmentioning

confidence: 99%

Oligosaccharide modification by swainsonine treatment inhibits pulmonary colonization by B16-F10 murine melanoma cells.

Humphries¹,

Matsumoto²,

White³

et al. 1986

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

165

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Oligosaccharide moieties of cell-surface glycoconijugates are thought to be involved in recognition events associated with tumor metastasis and invasion. Using swainsonine (SW), an inhibitor of Golgi a-mannosidase II that results in the formation of hybrid-type oligosaccharides on N-linked glycoproteins, we have tested the hypothesis that specific glycan structures are required for pulmonary colonization by tumor cells. B16-F10 murine melanoma cells were treated with SW in growth medium and then injected intravenously into syngeneic C57BL/6 mice. This treatment resulted in dramatic inhibition ofcolonization, but it had no effect on B16-F1O viability or on cellular tumorigenicity after subcutaneous implantation. SW-treated radiolabeled B16-F1O cells were cleared from the lungs at a greater rate than control cells, suggesting that one effect of treatment is to alter tumor cell retention in the target organ. Our results implicate specific glycan structures in pulmonary colonization and offer a potential approach for identification of specific macromolecules involved in tumor cell-organ recognition during metastasis. MD), and passaged twice weekly by short exposure to 0.25% trypsin/0.02% EDTA (GIBCO). Only cells <60 days old were used for these studies. Cultures were routinely tested for microbial infection and verified to be free of mycoplasma.Pulmonary Colonization. Six-week-old pathogen-free C57BL/6 mice (Charles River Breeding Laboratories, Wilmington, MA) were quarantined for 1 week and used over an age range of 8-10 weeks. SW was obtained either as a gift from H. P. Broquist (Vanderbilt University, Nashville, TN) or from Boehringer Mannheim and was dissolved in water.B16-F1O cells were plated at 106 or 5 x 105 cells per 75-cm2 flask and 2 or 3 days later, respectively, were treated with SW in growth medium for 18-22 hr. The just confluent cultures were then washed with divalent cation-free Dulbecco's phosphate-buffered saline (PBS-; GIBCO), detached with 0.02% EDTA for 2 min, and resuspended gently to 2.5 x 105 cells per ml in Dulbecco's MEM containing 10 mM 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid (GIBCO).Prior to injection, animals were warmed for 10 min to elicit vasodilation, and 0.2-ml aliquots of each cell suspension (containing 5 X 104 cells) were then injected slowly into the lateral tail vein as described by Fidler (19 The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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“…In a fibrosarcoma systcm a role was cstablished for cell surface et-galactosyl residucs in metastasis [119]. Enzymatic rcmoval of such residues compromiscd thc ability of the cells to attach to basement membrane components [120], whcreas the adhesion of metastatic rat hepatocarcinoma cells to monolaycrs of endothelial cells was inhibited by methyl ct-D-mannopyranoside and N-acetyI-D-galactosamine [121]. Thesc and other findings imply that carbohydrate recognition mechanisms may be responsible for some of thc cellular interactions that occur during the spread of metastatic tumor cells.…”

Section: Endogenous Surface Lectins On Host Cells and On Tumor Cells mentioning

confidence: 99%

Endogenous galactoside-binding lectins: a new class of functional tumor cell surface molecules related to metastasis

1987

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The formation of secondary tumors by circulating cancer cells (blood-borne metastasis) correlates with an increased tendency of the cells to form emboli by aggregation with other tumor cells or with host cells. Although it is evident that cell-cell recognition and adhesion are mediated by cell surface components, the identity of these molecules is only now being unraveled. Over the last decade an increasing number of studies have demonstrated the presence of endogenous carbohydrate-binding proteins on the surface of various normal cells, and it has been proposed that such lectin-like molecules might be involved in intercellular adhesion. We have shown that various tumor cell lines contain endogenous galactose-specific lectins. Lectin activity was detected at the cell surface by the binding of asialofetuin. This glycoprotein also enhanced the aggregation of the tumor cells. After purification by affinity chromatography on immobilized asialofetuin the lectin activity was associated with two proteins of Mr 14,500 and 34,000. By using polyclonal and monoclonal antilectin antibodies in conjunction with various immunologic techniques we have demonstrated that the endogenous lectins are present on the surface of different tumor cells. Quantitation of cell surface lectins by flow cytometric analyses of antilectin antibody binding revealed that among related tumor cells those exhibiting a higher metastatic potential expressed more lectin on their surface. The binding of monoclonal antilectin antibodies to metastatic cells decreased asialofetuin-induced homotypic aggregation in vitro and suppressed the ability of the cells to form lung metastases after intravenous injection in the tail vein of syngeneic mice. These results strongly implicate the tumor cell surface lectins in cell adhesion and metastasis. We propose that such lectins can increase the ability of tumor cells that enter the blood stream to form aggregates with other tumor cells, or to adhere to host cells or the extracellular matrix and thereby increase their metastatic potential. Other contributing components to tumor cell-host cell interactions are cell surface carbohydrate-binding proteins that have been detected on lymphocytes, platelets, macrophages, hepatocytes, and endothelial cells. These lectin-like molecules might recognize and bind carbohydrates expressed on the surface of tumor cells and enhance emboli formation and organ colonization.

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Contribution of α-d-galactopyranosyl end groups to attachment of highly and low metastatic murine fibrosarcoma cells to various substrates

Cited by 25 publications

References 22 publications

The role of tumor‐cell surface carbohydrate in experimental metastasis

The role of tumor‐cell surface carbohydrate in experimental metastasis

Oligosaccharide modification by swainsonine treatment inhibits pulmonary colonization by B16-F10 murine melanoma cells.

Endogenous galactoside-binding lectins: a new class of functional tumor cell surface molecules related to metastasis

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