Inflammatory cytokines stimulate the adhesion of colon carcinoma cells to mesothelial monolayers

Dig Dis Sci. 2007 Oct;52(10):2775-83. doi: 10.1007/s10620-007-9778-4. Epub 2007 Mar 30.

Abstract

Surgical handling of the peritoneum causes an inflammatory reaction, during which a potentially lethal cocktail of active mediators is produced, including cytokines and growth factors. The aim of this study was to investigate the effects of inflammatory cytokines on the interaction between tumor and mesothelial cells. Tumor cell adhesion to a mesothelial monolayer was assessed after preincubation of the mesothelium with interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha. Preincubation of the mesothelial monolayer with IL-1beta or TNF-alpha resulted in enhanced tumor cell adhesion of Caco2 and HT29 colon carcinoma cells. The amount of stimulation for the Caco2 cells was between 20% and 40% and for HT29 cells between 30% and 70%. Blocking experiments with anti-IL-1beta and anti-TNF-alpha resulted in significant inhibition of the cytokine-stimulated tumor cell adhesion. The presented results prove that IL-1beta and TNF-alpha are significant stimulating factors in tumor cell adhesion in vitro and may therefore account for tumor recurrence to the peritoneum in vivo.

MeSH terms

  • Adenocarcinoma / metabolism*
  • Adenocarcinoma / pathology
  • Caco-2 Cells
  • Cell Adhesion / physiology*
  • Cell Adhesion Molecules / genetics
  • Cell Adhesion Molecules / metabolism
  • Colonic Neoplasms / metabolism*
  • Colonic Neoplasms / pathology
  • DNA, Neoplasm / genetics
  • Gene Expression Regulation, Neoplastic
  • HT29 Cells
  • Humans
  • Immunohistochemistry
  • Interleukin-1beta / pharmacology*
  • Interleukin-6 / pharmacology*
  • Intestinal Mucosa / metabolism*
  • Intestinal Mucosa / pathology
  • Monocytes / metabolism
  • Monocytes / pathology
  • Receptors, Cytokine / genetics
  • Receptors, Cytokine / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Cell Adhesion Molecules
  • DNA, Neoplasm
  • Interleukin-1beta
  • Interleukin-6
  • Receptors, Cytokine
  • Tumor Necrosis Factor-alpha