It has been generally accepted for 20 years that the growth of Shionogi
carcinoma 115 (SC115) is stimulated only by
androgen. However, we recently found that the growth of SC115 cells is also stimulated by pharmacological doses of
estrogen in vivo but not in cell culture. In the present study, the growth-stimulatory effect of
glucocorticoid on SC115 cells was examined. In castrated mice, daily
injections of high doses of
dexamethasone (100 micrograms/mouse) markedly stimulated the
tumor growth, and the growth approached that found in normal males. However, daily
injections of physiological doses of
dexamethasone (4 micrograms/mouse) or high doses of
epitestosterone,
progesterone, or
cholesterol (200-5000 micrograms/mouse) did not enhance the
tumor growth in castrated mice. The
androgen dependency, growth speed,
steroid receptors, and histological type of the
tumors grown by pharmacological doses of
glucocorticoid were not significantly different from those of the original SC115
tumors grown by
androgen. In a serum-free medium [Ham's F-12:Eagle's minimum essential medium (1:1, v/v) containing 0.1%
bovine serum albumin], the proliferation of SC-3 cells (a cloned cell line from SC115 cells) was markedly (by up to 25-fold) stimulated by 10(-10)-10(-8) M
testosterone, whereas the proliferation was only slightly but significantly (by up to 3.3-fold) stimulated by 10(-8)-10(-5) M
dexamethasone. The present findings demonstrate that the growth of SC115 cells in vivo and in cell culture is significantly stimulated by physiological doses of
androgen or pharmacological doses of
glucocorticoid.