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

J Cancer Res Clin Oncol. 1988;114(2):217-20. doi: 10.1007/BF00417842.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1-Deoxynojirimycin
  • Alkaloids / pharmacology*
  • Animals
  • Carbohydrates / analysis
  • Cyclohexenes
  • Glucosamine / analogs & derivatives
  • Glucosamine / pharmacology
  • Glycoproteins / analysis*
  • Glycoproteins / physiology*
  • Inositol / analogs & derivatives*
  • Inositol / pharmacology
  • Lung Neoplasms / secondary*
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Sarcoma, Experimental / pathology*
  • Swainsonine
  • Tunicamycin / pharmacology*

Substances

  • Alkaloids
  • Carbohydrates
  • Cyclohexenes
  • Glycoproteins
  • Tunicamycin
  • 1-Deoxynojirimycin
  • 6-bromoconduritol
  • Inositol
  • Glucosamine
  • Swainsonine