Glycoprotein modifications of sarcoma L-1 tumor cells by tunicamycin, swainsonine, bromoconduritol or 1-desoxynojirimycin treatment inhibits their metastatic lung colonization in Balb/c-mice

Synthesis and expression of cell surface carbohydrates appear to be involved in recognition events associated with tumor invasion and metastasis. Thus, the potential of murine sarcoma L-1 cells to form experimental lung metastases after i.v. injection was assessed after inhibiting tumor cell protein...

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Bibliographic Details
Published in:Journal of cancer research and clinical oncology 1988-01, Vol.114 (2), p.217-220
Main Authors: PULVERER, G, BEUTH, J, KO, H. L, YASSIN, A, OHSHIMA, Y, ROSZKOWSKI, K, UHLENBRUCK, G
Format: Article
Language:English
Subjects:
1-Deoxynojirimycin
Alkaloids - pharmacology
Animals
Antineoplastic agents
Biological and medical sciences
Carbohydrates - analysis
Cyclohexenes
General aspects
Glucosamine - analogs & derivatives
Glucosamine - pharmacology
Glycoproteins - analysis
Glycoproteins - physiology
Inositol - analogs & derivatives
Inositol - pharmacology
Lung Neoplasms - secondary
Male
Medical sciences
Mice
Mice, Inbred BALB C
Pharmacology. Drug treatments
Sarcoma, Experimental - pathology
Swainsonine
Tunicamycin - pharmacology
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Summary:Synthesis and expression of cell surface carbohydrates appear to be involved in recognition events associated with tumor invasion and metastasis. Thus, the potential of murine sarcoma L-1 cells to form experimental lung metastases after i.v. injection was assessed after inhibiting tumor cell protein glycosylation with tunicamycin, swainsonine, bromoconduritol, or 1-desoxynojirimycin. Incubation of sarcoma L-1 cells with 0.5 microgram (or above) of these substances/ml medium for 20-24 h significantly inhibited lung colonization. Cytotoxic side effects or additional organ manifestations could not be found. Gas liquid chromatographic examinations of carbohydrates from treated L-1 cells indicated that sugar synthesis was evidently inhibited. These results suggest that specific glycan structures on tumor cells are required for expression of the metastatic phenotype.
ISSN:0171-5216
1432-1335
DOI:10.1007/BF00417842