Modification of blood-borne arrest properties of lymphoma cells by inhibitors of protein glycosylation suggests the existence of endogenous lectins

Schaaf‐Lafontaine, Nicole; Hooghe, Robert; Plaetse, F. Vander

doi:10.1016/0008-6215(85)85114-4

Cited by 22 publications

(4 citation statements)

References 23 publications

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“…The relationship between the cell lines for endothelial cell adhesion, organ retention and organ colonization was consistent and proportionate: MDAY-D2 > Gal-D36W25 > D36W25. Swainsonine-and castinospermine-treated MDAY-D2 cells were also intermediate between MDAY-D2 and D36W25 for adhesion to endothelial ceils in vitro, and, as previously shown, the drugs inhibit organ retention and colonization (Schaaf-Lafontaine, 1985;Humphries et al, 1986;Dennis, 1986b). Since galactosylation of mutant D36W25 cells does not completely restore endothelial cell adhesion and organ retention to the level observed for wild-type MDAY-D2 cells, it is likely that more complex sequences containing B1-4Gal participate in MDAY-D2 adhesion to endothelium.…”

Section: Discussionsupporting

confidence: 76%

Tumor cell surface beta 1-4-linked galactose binds to lectin(s) on microvascular endothelial cells and contributes to organ colonization.

Cornil

Kerbel

Dennis

1990

The Journal of Cell Biology

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Abstract. Cell surface carbohydrate structures acting as ligands for tissue specific mammalian lectins have been implicated in cell-cell interactions during embryogenesis, lymphocyte homing, and tumor cell metastasis. In this report, we provide evidence that /31-4 linked galactose (Gal) residues in N-linked oligosaccharides on the surface of blood born tumor cells serve as a ligand for binding to microvascular endothelial cells. D36W25, a class 1 glycosylation mutant of the MDAY-D2 lymphoreticular tumor cell line, lacks sialic acid and Gal in cellular glycans due to a defect in the Golgi UDP-Gal transporter. Using UDPGal and bovine galactosyltransferase in vitro, ill-4 Gal was restored to the surface of the cells and 70% of the galactosylated glycans persisted for 8 h in vitro at 37°C. Compared to mock-treated D36W25 cells, galactosylated D36W25 ceils showed an 80% increase in binding to microvascular endothelial cell monolayers in vitro. The enhanced binding of galactosylated D36W25 cells to endothelial cell was inhibited by the addition of lactosamine-conjugated albumin to the assay. Consistent with these observations, swainsonine and castinospermine, two inhibitors of N-linked processing that result in loss of lactosamine antennae inhibited the binding of wild-type MDAY-D2 cells to endothelial cells in vitro. Injection of radiolabeled tumor cells into the circulation of syngeneic mice, showed that galactosylation of D36W25 cells resulted in 2-3 more tumor cells retained in the lungs and livers. In addition, galactosylation of D36W25 cells increased by 30-fold the number of visible liver metastases on inspection 4 wk after tumor cell injection. These results suggest that fll-4Gal-binding lectins on microvascular endothelial cells can contribute to retention and secondary tumor formation of blood born tumor cells. With the increasing availability of purified glycosyltransferases, reconstruction of a variety of carbohydrate sequences on the surface of class 1 mutants provides a controlled means of studying carbohydratelectin interactions on viable cells.

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Section: Discussionsupporting

confidence: 76%

Tumor cell surface beta 1-4-linked galactose binds to lectin(s) on microvascular endothelial cells and contributes to organ colonization.

Cornil

Kerbel

Dennis

1990

The Journal of Cell Biology

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“…Circumstantial evidence includes the ability to: select metastatic cell variants with altered surface glycoproteins [87,92] and endogenous lectin-binding site variants with modified metastatic properties [171,172]; inhibit experimental metastasis by pretreatment of malignant cells with anti-endogenous lectin MAb [171,173]; and remove cell surface terminal saccharides with specific enzymes and their effect on metastasis formation [174]. In addition, the presence of endogenous lectins on various metastatic tumor cells and the amounts of cell surface sialo-and other glycoconjugates also correlate with metastatic potential [115][116][117][118][171][172][173][174][175][176][177][178][179], and abrogation of tumor cell metastatic and endothelial cell-binding properties can be affected by metabolic alterations in tumor cell surface oligosaccharides [180,181]. To demonstrate an association with metastasis, Meromsky et al [173] used a MAb directed against the endogenous galactoside-specific lectin of murine melanomas and fibrosarcomas.…”

Section: Tumor Cell-endothelial Cell Interactionsmentioning

confidence: 99%

Organ specificity of tumor metastasis: role of preferential adhesion, invasion and growth of malignant cells at specific secondary sites

1988

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The locations of distant secondary tumors in many clinical cancers and animal tumors are nonrandom, and their distributions cannot be explained by simple anatomical or mechanical hypotheses based on the simple lodgment or trapping of tumor cell cmboli in the first capillary bed encountered. Evidence from certain experimental tumor systems supports Paget's 'seed and soil' hypothesis on the nonrandom distributions of metastases, in which the unique properties of particular tumor ceils ('seeds') and the different characteristics of each organ microenvironment ('soil') collectively determine the organ preference of metastasis. Experimentally, differential tumor cell adhesion to organ-derived microvessel endothelial cells and organ parenchymal cells, differential invasion of basement membranes and organ tissues, and differential responses to organ-derived growth-stimulatory and -inhibitory factors all appear to be important determinants in explaining the organ preference of metastasis. Each tumor system may achieve organ specificity because of its own unique set of multiple metastasis-associated properties and responses to host microenvironments. As neoplasms progress to more highly malignant states multisite metastases are more likely and organ-specific metastases may be masked or circumvented owing to stochastic events, tumor cell diversification, host selection processes, and increased production of tumor autocrine molecules that may modulate adhesion, invasion, growth, and other properties important in metastasis. The importance of each of these properties, however, appears to vary considerably among different metastatic tumor systems. These and other tumor cell and host properties may eventually be used to predict and explain the unique metastastic distributions of certain human malignancies.

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“…injection into the tail vein of syngeneic mice [114]. Similarly, the blood-borne arrest of lymphoma cells in the spleen was scnsitive to treatments interfcring with thc processing of N-linked oligosaccharides (e.g., swainsonine and deoxynojirimycin), or to ncuraminidase [115]. Surface sialic acid was implicd to play a role in metastasis [116[ and attachment of metastatic cells to collagen type IV and fibronectin [117].…”

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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Modification of blood-borne arrest properties of lymphoma cells by inhibitors of protein glycosylation suggests the existence of endogenous lectins

Cited by 22 publications

References 23 publications

Tumor cell surface beta 1-4-linked galactose binds to lectin(s) on microvascular endothelial cells and contributes to organ colonization.

Tumor cell surface beta 1-4-linked galactose binds to lectin(s) on microvascular endothelial cells and contributes to organ colonization.

Organ specificity of tumor metastasis: role of preferential adhesion, invasion and growth of malignant cells at specific secondary sites

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

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