The role of glycoconjugates in metastatic melanoma blood‐borne arrest and cell surface properties

Irimura, Tatsuro; Nicolson, Garth L.

doi:10.1002/jsscb.380170404

Cited by 32 publications

(8 citation statements)

References 56 publications

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“…As other authors have found [22,34,33], tumor cell adherence to ECM was more efficient than attachment to endothelial cells. The percentages of tumor cells bound to endothelial cell monolayers and to ECM were similar to those obtained by Vlodavsky et al [23].…”

Section: Discussionsupporting

confidence: 54%

Cellular Functions Related to Metastasis Differing between Low- and High-Malignancy Variants of AKR Lymphoma

Klein

Savion²,

Staroselsky³

et al. 1992

Pathobiology

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Two AKR lymphoma variants of low (LM) and high (HM) malignancy were characterized for cell properties important for metastatic capacity. Previous data suggested that these murine lymphoma variants differed in the late phase of metastasis. In the present study we attempted to determine more accurately the stage in which they differ. The HM cells attached less efficiently than the LM ones to both endothelial cells (5 times) and extracellular matrix (twice), possibly indicating a more efficient extravasation capacity of the HM cells. The level of heparinase was low in the two variant cells. Attachment to liver sections was, however, more efficient with the HM than with the LM cells.

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Section: Discussionsupporting

confidence: 54%

Cellular Functions Related to Metastasis Differing between Low- and High-Malignancy Variants of AKR Lymphoma

Klein

Savion²,

Staroselsky³

et al. 1992

Pathobiology

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“…For example, Irimura and Nicolson (138) found that treatment of B16 melanoma cells with tunicamycin, an inhibitor of glycoprotein synthesis, altered their arrest pattern in vivo following i.v. injection and impaired their ability to produce lung metastates.…”

Section: B Experimental Models For Studying the Behavior Of Circulatmentioning

confidence: 99%

Experimental systems for analysis of the malignant phenotype

Poste

1982

Cancer Metast Rev

109

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Identification of the cellular and subcellular alterations responsible for the metastatic behavior of malignant tumor cells and development of reliable screening programs for detecting new therapeutic agents for improved treatment of metastatic disease both depend crucially on the availability of experimental systems that can serve as relevant models of human cancer. Recent advances in our understanding of the pathogenesis of cancer metastasis have raised serious doubts about the usefulness of many of the experimental approaches that have long been used in the study of metastasis. Recent findings showing that metastases are caused by specific subpopulations of metastatic tumor cells, and that not all cells in a malignant primary tumor possess metastatic properties, are of profound importance for experimental efforts to understand the mechanism of metastatic phenotype among cells from the same tumor means that the traditional, and widely used, approach of analyzing primary tumors and cultured cell lines containing multiple, phenotypically heterogeneous, subpopulations of cells may provide little or no insight into the properties of the metastatic subpopulations, particularly if they represent only a minor fraction of the entire population. Similarly, the practice of screening potential therapeutic modalities for their ability to reduce the mass and/or growth rate of a primary tumor may be inadequate in predicting the responsiveness of metastatic lesions. Solution of these problems requires that new methods must be devised to isolate and characterize the specific subpopulations of tumor cells endowed with metastatic potential. In addition, knowledge of how the extraordinary phenotypic diversity found in tumor cell subpopulations from the same tumor is generated and how subpopulation diversity is regulated during progressive growth of both the primary tumor and its metastases are of fundamental importance if we are to design meaningful experimental systems for studying the metastatic process. This article reviews our current understanding of these complex issues and their implications for the experimental analysis of the malignant phenotype. The merits and shortcomings of different experimental systems are discussed in detail together with the identification of areas in which new experimental strategies and models are now needed.'

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“…This effect has been correlated with the presence of certain surface sialoglycoproteins (8,9,11). However, since tunicamycin is known to be toxic at least for most tumor cells (12,13), the significance of this finding remains unclear.…”

mentioning

confidence: 92%

“…In assays for blood-borne metastasis, treatment of B16 murine melanoma cells with tunicamycin, an inhibitor of the biosynthesis of N-linked glycoproteins, appeared to abrogate pulmonary colonization in syngeneic mice (8)(9)(10). This effect has been correlated with the presence of certain surface sialoglycoproteins (8,9,11).…”

mentioning

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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The role of glycoconjugates in metastatic melanoma blood‐borne arrest and cell surface properties

Cited by 32 publications

References 56 publications

Cellular Functions Related to Metastasis Differing between Low- and High-Malignancy Variants of AKR Lymphoma

Cellular Functions Related to Metastasis Differing between Low- and High-Malignancy Variants of AKR Lymphoma

Experimental systems for analysis of the malignant phenotype

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

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