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Opioid alkaloids and casomorphin peptides decrease the proliferation of prostatic cancer cell lines (LNCaP, PC3 and
M Kampa1, E Bakogeorgou, A Hatzoglou
1Laboratory of Experimental Endocrinology, University of Crete, School of Medicine and University Hospital, Heraklion, Greece.
European Journal of Pharmacology
|November 22, 1997
Summary
Opioid agonists and casomorphin peptides inhibit prostate cancer cell growth. These compounds act via specific opioid receptors and other membrane receptors, suggesting a role for opioids in prostate cancer progression.
Area of Science:
- Oncology
- Pharmacology
- Cell Biology
Background:
- Prostate cancer cell proliferation is a critical factor in disease progression.
- The role of opioid signaling in cancer remains an area of active investigation.
- Opioid receptors have been identified in various non-neuronal tissues, including the prostate.
Purpose of the Study:
- To investigate the effect of opioid agonists and casomorphin peptides on human prostate cancer cell lines.
- To elucidate the mechanisms underlying the observed effects, including the involvement of opioid receptors.
Main Methods:
- Treatment of LNCaP, DU145, and PC3 human prostate cancer cell lines with various opioid agonists and casomorphin peptides.
- Dose-response studies to determine 50% inhibitory concentrations (IC50).
- Experiments using the opioid antagonist diprenorphine to assess receptor involvement.
- Saturation binding experiments with selective ligands to characterize opioid receptor subtypes.
Main Results:
- Opioid agonists (ethylketocyclazocine, etorphine, [D-Ala2,D-Leu5]enkephalin (DADLE), [D-Ala2, N-Me-Phe4-Gly-ol]enkephalin (DAGO), [D-Ser2,Leu5]enkephalin-Thr6 (DSLET), and morphine) inhibited prostate cancer cell proliferation in a dose-dependent manner with picomolar IC50 values.
- The inhibitory effects were partially antagonized by diprenorphine, suggesting specific opioid receptor involvement in PC3 and DU145 cell lines (kappa1, mu, and kappa3 sites identified).
- Casomorphin peptides derived from bovine and human caseins also inhibited prostate cancer cell proliferation, with mechanisms partly involving opioid receptors.
Conclusions:
- Opioid agonists and casomorphin peptides exhibit potent inhibitory effects on human prostate cancer cell proliferation.
- These findings highlight a potential role for opioid signaling, both endogenous and exogenous, in modulating prostate cancer growth.
- The presence of opioid receptors in prostate cancer cells suggests therapeutic opportunities for targeting opioid pathways in prostate cancer treatment.