Interleukin-1 blocks insulin and insulin-like growth factor-stimulated growth in MCF-7 human breast cancer cells by inhibiting receptor tyrosine kinase activity

Endocrinology. 1996 Oct;137(10):4100-7. doi: 10.1210/endo.137.10.8828463.

Abstract

Interleukins-1 (IL-1s) are known to inhibit the growth of cultured breast cancer cells. We examined the effects of IL-1 alpha and IL-1 beta on insulin and insulin-like growth factor I (IGF-I) stimulation of cell growth and found that both IL-1s inhibited anchorage-dependent and independent growth of MCF-7 breast cancer cells. In cells incubated with IL-1 beta (100 U/ml), insulin receptor (IR) protein and messenger RNA were increased by 100%, while IGF-I receptor protein and transcript were not significantly changed. These data were confirmed by binding studies. Incubation of MCF-7 cells with IL-1s led, however, to a significant inhibition of IR and IGF-I receptor autophosphorylation (-55%) and phosphotransferase activity (-65%). Also, in 3T3/ HIR rat fibroblasts, transfected with and overexpressing IR, IL-1s decreased insulin-stimulated cell growth in soft agar and IR tyrosine kinase activity. The present findings suggest that IL-1s antagonize the insulin and IGF-I mitogenic effects in MCF-7 cells by blocking the receptor tyrosine kinase activity that is crucial for the mitogenic effect of these factors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells / metabolism
  • Animals
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology*
  • Cell Division / drug effects
  • Humans
  • Insulin / pharmacology*
  • Insulin-Like Growth Factor I / metabolism
  • Insulin-Like Growth Factor I / pharmacology*
  • Interleukin-1 / pharmacology*
  • Mice
  • RNA, Messenger / metabolism
  • Rats
  • Receptor Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Receptor, Insulin / drug effects
  • Receptor, Insulin / genetics
  • Receptor, Insulin / metabolism
  • Receptors, Somatomedin / drug effects
  • Receptors, Somatomedin / genetics
  • Receptors, Somatomedin / metabolism
  • Recombinant Proteins
  • Tumor Cells, Cultured

Substances

  • Insulin
  • Interleukin-1
  • RNA, Messenger
  • Receptors, Somatomedin
  • Recombinant Proteins
  • Insulin-Like Growth Factor I
  • Receptor Protein-Tyrosine Kinases
  • Receptor, Insulin