We investigated the effects of dihydrotestosterone (DHT), hydrocortisone (HC), basic fibroblast growth factor (bFGF), and opioid peptides on the growth of cells from the androgen-responsive Shionogi mouse mammary carcinoma (SC115) in primary culture. Androgen-responsive SC115 tumor cells were stimulated to grow in response to DHT, HC, and bFGF in a dose-responsive manner in both serum-containing and serum-free media. Moreover, anti-bFGF antibody had a marked inhibitory effect on DHT- and bFGF-induced growth. Three opioid agonists, β-endorphin (β-EP), cyclazocine, and morphine sulfate, markedly inhibited SC115 tumor cell growth at concentrations ranging from 10-11 to 10-7m in serumcontaining medium with or without DHT, HC, or bFGF, with the greatest inhibition occurring in medium with DHT. In serum-free medium, β-EP had no inhibitory effects on cell growth. However, β-EP at concentrations of 10-9m or greater significantly inhibited cell growth in serum-free medium containing DHT, HC, or bFGF, with the greatest inhibition again occurring in medium with DHT. Naloxone (10-8 and 10-6m), an opioid receptor antagonist, blocked the inhibitory effects of β-EP and morphine sulfate. These results suggest that SC115 tumor cells in primary culture are stimulated to grow in a dose-responsive manner by DHT, HC, or bFGF in both serum-containing and serum-free media. It appears that bFGF may mediate, at least partially, DHT-stimulated cell growth. In addition, the opioid peptide system may be involved in regulating endocrine control of growth of the androgen-responsive SC115 carcinoma. The dose-responsive inhibitory effects of opioids and their reversal by naloxone suggest that these effects may be mediated by opioid receptors.

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This research was supported by grants obtained from the British Columbia Health Research Foundation and the Medical Research Council of Canada.

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