Inhibitory effect of antibody against basic fibroblast growth factor on androgen- or glucocorticoid-induced growth of Shionogi carcinoma 115 cells in serum-free culture.
Shionogi carcinoma 115 (SC115) has been accepted for 20 years as an androgen-responsive mouse mammary tumor. However, we and others recently found that the growth of SC115 cells is also stimulated by high doses of glucocorticoids. We already reported the following findings. In a serum-free medium [Ham's F-12: Eagle's minimum essential medium (1:1, v/v) containing 0.1% bovine serum albumin], greater than or equal to 10(-9) M testosterone and greater than or equal to 10(-8) M dexamethasone significantly stimulated the growth of SC-3 cells (a cloned cell line from a SC115 tumor) through androgen and glucocorticoid receptors, respectively. In the present study, we have demonstrated that higher concentrations (10(-7)-10(-6) M) of weak androgens such as 4-androstene-3,17-dione or weak glucocorticoids such as corticosterone also significantly stimulate the growth of SC-3 cells and that their relative potency is found to be in parallel with their binding affinity for their receptors, respectively. Furthermore, DNA synthesis of SC-3 cells induced by 0.1 ng/ml basic fibroblast growth factor (FGF), 10(-8) M testosterone, 10(-6) M 4-androstene-3,17-dione, 10(-7) M dexamethasone, or 10(-6) M corticosterone was found to be similarly and significantly inhibited by the addition of basic FGF neutralizing antibody IgG in the present study; approximately 70% inhibition of the basic FGF, androgen, or glucocorticoid effects was attained. We already reported findings which suggest that SC-3 cells produce FGF-like peptide for their testosterone-induced growth. Therefore, the present study presents new additive information to demonstrate that the growth-stimulatory activity of various androgens or possibly glucocorticoids on SC-3 cells is mediated through a FGF-like peptide in an autocrine mechanism.
Lu
J
J
Department of Pathology, Osaka University Medical School, Japan.
Nishizawa
Y
Y
Tanaka
A
A
Nonomura
N
N
Yamanishi
H
H
Uchida
N
N
Sato
B
B
Matsumoto
K
K
D000735:Androstenedione / Q000494:pharmacology*; D000818:Animals; D000906:Antibodies; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D002999:Clone Cells; D003345:Corticosterone / Q000494:pharmacology*; D003470:Culture Media; D004261:DNA Replication; D003907:Dexamethasone / Q000494:pharmacology*; D005346:Fibroblast Growth Factors / Q000276:immunology / Q000494:pharmacology / Q000502:physiology*; D007700:Kinetics; D008325:Mammary Neoplasms, Experimental / Q000378:metabolism / Q000473:pathology*; D051379:Mice; D011944:Receptors, Androgen / Q000378:metabolism; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D013739:Testosterone / Q000494:pharmacology*
D000906:Antibodies; D003470:Culture Media; D011944:Receptors, Androgen; D011965:Receptors, Glucocorticoid; D013739:Testosterone; D000735:Androstenedione; D005346:Fibroblast Growth Factors; D003907:Dexamethasone; D003345:Corticosterone