Abstract
In the present study, we investigated the action of opioid receptor agonists on the proliferation of cells of the T47D human breast cancer cell line, grown in the absence of exogenously added steroids and growth factors. We found that the opioid receptor agonists ethylketocyclazocine, morphine, [ d-Ala 2, d-Leu 5]enkephalin (DADLE), [ d-Ser 2,Leu 5]enkephalin-Thr 6 (DSLET) and etorphine inhibit dose dependently cell proliferation. The opioid receptor antagonist diprenorphine had no significant effect per se, but it was able to reverse the action of all opioid receptor agonists except morphine. In order to investigate the mechanism of action of opioids on T47D cells, we characterised the opioid receptors present on this cell line, by saturation binding, using radiolabelled [ d-Ala 2, N-Me-Phe 4-Gly 5-ollenkephalin (DAGO, μ-opioid receptor agonist), ethylketocyclazocine ( κ 1-, κ 2-, μ- and δ-opioid receptor agonist), diprenorphine ( κ 2-, κ 3-, δ- and μ-opioid receptor antagonist), DADLE ( δ- and μ-opioid receptor agonist), and effectors. We identified opioid binding sites belonging mainly to the κ-type ( κ 1, κ 2 and κ 3), a few δ-opioid receptor sites, but no μ-opioid receptors. Our results indicate that the inhibitory effect of opioids on T47D cell growth is mediated through κ- and δ-opioid receptors. The effect of μ-acting morphine might not be mediated through opioid receptors.
Published Version
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