title: Effects of steroid hormones and opioid peptides on the growth of androgen-responsive Shionogi carcinoma (SC115) cells in primary culture.
abstract: 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, beta-endorphin (beta-EP), cyclazocine, and morphine sulfate, markedly inhibited SC115 tumor cell growth at concentrations ranging from 10(-11) to 10(-7) M in serum-containing medium with or without DHT, HC, or bFGF, with the greatest inhibition occurring in medium with DHT. In serum-free medium, beta-EP had no inhibitory effects on cell growth. However, beta-EP at concentrations of 10(-9) M 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(-6) M), an opioid receptor antagonist, blocked the inhibitory effects of beta-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.
authors.affiliation: Department of Anatomy, University of British Columbia, Vancouver, Canada.
authors.forename: Y
authors.initials: Y
authors.lastname: Jiang
authors.forename: J
authors.initials: J
authors.lastname: Weinberg
authors.forename: D A
authors.initials: DA
authors.lastname: Wilkinson
authors.forename: J T
authors.initials: JT
authors.lastname: Emerman
mesh_terms: D000818:Animals; D002455:Cell Division / Q000187:drug effects; D013196:Dihydrotestosterone / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000494:pharmacology*; D006854:Hydrocortisone / Q000494:pharmacology*; D008297:Male; D008325:Mammary Neoplasms, Experimental / Q000473:pathology*; D051379:Mice; D009270:Naloxone / Q000494:pharmacology; D009294:Narcotics / Q000494:pharmacology*; D014407:Tumor Cells, Cultured
chemical_list: D009294:Narcotics; D013196:Dihydrotestosterone; D016222:Fibroblast Growth Factor 2; D009270:Naloxone; D006854:Hydrocortisone