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.

Abstract

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.