Inhibition of cell motility after nm23 transfection of human and murine tumor cells

Cancer Res. 1993 May 1;53(9):1971-3.

Abstract

Abstract nm23 gene expression has been inversely correlated with tumor metastatic potential in certain tumors including melanomas, breast carcinomas, and hepatocellular carcinomas. The cellular mechanisms by which the nm23 protein may directly or indirectly modulate the metastatic phenotype is not yet known. Because cell motility plays an essential role in metastatic dissemination, we have studied whether tumor cells transfected with nm23 complementary DNA have any alterations in their ability to migrate. Our results demonstrate that nm23 transfection inhibits the ability of murine melanoma and human breast carcinoma cells to migrate in response to serum or to defined factors such as platelet derived growth factor or insulin-like growth factor 1. Random, unstimulated cell motility was not depressed in the nm23 transfectants. The results suggest that the nm23 gene product may interact with intracellular molecules that are essential for stimulated cell motility in two different tumor cell systems.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cell Movement*
  • Humans
  • Insulin-Like Growth Factor I / pharmacology
  • Mice
  • Monomeric GTP-Binding Proteins*
  • NM23 Nucleoside Diphosphate Kinases
  • Nucleoside-Diphosphate Kinase*
  • Platelet-Derived Growth Factor / pharmacology
  • Proteins / physiology*
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transcription Factors*
  • Transfection
  • Tumor Cells, Cultured

Substances

  • NM23 Nucleoside Diphosphate Kinases
  • Platelet-Derived Growth Factor
  • Proteins
  • Transcription Factors
  • Insulin-Like Growth Factor I
  • NME1 protein, human
  • Nme1 protein, mouse
  • Nucleoside-Diphosphate Kinase
  • Monomeric GTP-Binding Proteins
  • Tetradecanoylphorbol Acetate