Effect of a synthetic cannabinoid agonist on the proliferation and invasion of gastric cancer cells

J Cell Biochem. 2010 May 15;110(2):321-32. doi: 10.1002/jcb.22540.

Abstract

Although cannabinoids are associated with antineoplastic activity in a number of cancer cell types, the effect in gastric cancer cells has not been clarified. In the present study, we investigated the effects of a cannabinoid agonist on gastric cancer cell proliferation and invasion. The cannabinoid agonist WIN 55,212-2 inhibited the proliferation of human gastric cancer cells in a dose-dependent manner and that this effect was mediated partially by the CB(1) receptor. We also found that WIN 55,212-2 induced apoptosis and down-regulation of the phospho-AKT expression in human gastric cancer cells. Furthermore, WIN 55,212-2 treatment inhibited the invasion of gastric cancer cells, and down-regulated the expression of MMP-2 and VEGF-A through the cannabinoid receptors. Our results open the possibilities in using cannabinoids as a new gastric cancer therapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects
  • Base Sequence
  • Benzoxazines / pharmacology*
  • Cell Line, Tumor
  • Cell Proliferation / drug effects*
  • DNA Primers
  • Down-Regulation / drug effects
  • Flow Cytometry
  • Humans
  • Immunohistochemistry
  • Morpholines / pharmacology*
  • Naphthalenes / pharmacology*
  • Neoplasm Invasiveness / prevention & control*
  • Receptor, Cannabinoid, CB1 / agonists*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Stomach Neoplasms / pathology*

Substances

  • Benzoxazines
  • DNA Primers
  • Morpholines
  • Naphthalenes
  • Receptor, Cannabinoid, CB1
  • Win 55212-2