Breast cancer cell-derived cytokines, macrophages and cell adhesion: implications for metastasis

Anticancer Res. 2011 Oct;31(10):3219-27.

Abstract

Background: Liver metastasis is associated with a proinflammatory microenvironment and up-regulation of cell adhesion molecules expressed by endothelial cells. The aim of this study was to characterize the interrelations between breast cancer cell-secreted cytokines, macrophages and E-selectin-mediated cancer cell adhesion and their role in metastasis of breast cancer.

Materials and methods: Three metastatic breast cancer cell lines (1590, KM22, ZE) were studied. Cell culture supernatants were screened for cytokines and the potential for cytokines to increase tumor-necrosis factor-α (TNF-α) production by ANA-1-macrophages was analyzed. E-Selectin-mediated tumor cell adhesion of fluorescence labelled tumor cells was evaluated by measurement of fluorescence intensity with and without E-selectin-blocking strategies (monoclonal antibodies, cimetidine).

Results: Tumor-specific cytokine secretion patterns were revealed. TNF-α secretion from cultured macrophages increased after incubation with tumor supernatants. Tumor cell adhesion was significantly inhibited by cimetidine and monoclonal antibodies against E-selectin (KM22 with cimetidine, p<0.05).

Conclusion: Breast cancer cell-secreted cytokines stimulate macrophages to produce TNF-α, a known up-regulator of E-selectin expression, and therefore cell adherence to endothelium. Inhibition of this mechanism could be an attractive therapeutic option for the prevention of breast cnacer metastasis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal / pharmacology
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology*
  • Cell Adhesion / drug effects
  • Cell Line, Tumor
  • Cimetidine / pharmacology
  • Cytokines / metabolism*
  • E-Selectin / immunology
  • Endothelial Cells / cytology
  • Endothelial Cells / drug effects
  • Endothelial Cells / metabolism
  • Female
  • Humans
  • Macrophages / drug effects
  • Macrophages / metabolism
  • Macrophages / pathology*
  • Mice
  • Neoplasm Metastasis / pathology*
  • Solubility / drug effects
  • Subcellular Fractions / drug effects
  • Subcellular Fractions / metabolism
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Umbilical Veins / cytology
  • Up-Regulation / drug effects

Substances

  • Antibodies, Monoclonal
  • Cytokines
  • E-Selectin
  • Tumor Necrosis Factor-alpha
  • Cimetidine