Paracrine interactions between mesothelial and colon-carcinoma cells in a rat model

Int J Cancer. 1997 Dec 10;73(6):885-90. doi: 10.1002/(sici)1097-0215(19971210)73:6<885::aid-ijc21>3.0.co;2-2.

Abstract

This study used a co-culture system with Transwell tissue-culture inserts to investigate the role of primary cultures of rat peritoneal mesothelial cells on the proliferation of rat colon-carcinoma cells (CC531 cells). Mesothelial cells significantly inhibited the growth of CC531 cells, while, conversely, CC531 cells stimulated the growth of mesothelial cells. Receptor-binding studies demonstrated the presence of high-affinity IGF-I receptors on the mesothelial and CC531 cells. Both cell types also produced IGF-I, as measured by radioimmunoassay. IGF-I stimulated DNA synthesis in mesothelial cells, but had no effect on the growth of CC531 cells. In co-culture, it was found that IGF-I potentiated the inhibitory effect of mesothelial cells on CC531 cells. The effect of IGF-I on mesothelial-cell proliferation was additive to the stimulatory effect of CC531 cells. TGF-beta had no effect on the growth of the CC531 cells, suggesting that this growth (-inhibitory) factor is not involved in the inhibitory effect of mesothelial cells on CC531 cell growth. The study provides evidence for the existence of a paracrine loop between mesothelial and colon-carcinoma cells, giving more insight into the basic cellular mechanisms that may modulate the growth of intraperitoneal colon carcinoma. Inhibition of CC531-cell proliferation by rat mesothelial cells might explain the earlier finding that tumour cells grow poorly in a surgically uncompromised abdomen.

MeSH terms

  • Animals
  • Cell Division
  • Cells, Cultured
  • Coculture Techniques
  • Colonic Neoplasms / metabolism
  • Colonic Neoplasms / pathology
  • Colonic Neoplasms / physiopathology*
  • Culture Media, Conditioned
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Epithelial Cells / cytology
  • Epithelial Cells / metabolism
  • Epithelial Cells / physiology*
  • Immunohistochemistry
  • Insulin-Like Growth Factor I / metabolism
  • Insulin-Like Growth Factor I / pharmacology
  • Keratins / analysis
  • Male
  • Paracrine Communication*
  • Rats
  • Rats, Inbred Strains
  • Receptor, IGF Type 1 / metabolism
  • Transforming Growth Factor beta / pharmacology
  • Tumor Cells, Cultured
  • Vimentin / analysis
  • von Willebrand Factor / metabolism

Substances

  • Culture Media, Conditioned
  • Transforming Growth Factor beta
  • Vimentin
  • von Willebrand Factor
  • Insulin-Like Growth Factor I
  • Keratins
  • Receptor, IGF Type 1