| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Departments of Pathology [Y. O., N. N., D. H., Y. N., K. M.] and Internal Medicine [B. S.], Osaka University Medical School, Kita-ku, Osaka 530; Shionogi Research Laboratory [N. U.], Fukushima-ku, Osaka 553; and Department of Surgery, The Center for Adult Diseases [S. N.], Higashinari-ku, Osaka 537, Japan
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 µg/mouse) markedly stimulated the tumor growth, and the growth approached that found in normal males. However, daily injections of physiological doses of dexamethasone (4 µg/mouse) or high doses of epitestosterone, progesterone, or cholesterol (2005000 µg/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.
1 Supported in part by a Grant-in-Aid for Cancer Research from the Ministry of Education, Science and Culture, and by a grant from the Japanese Foundation for Multidisciplinary Treatment of Cancer.
2 To whom requests for reprints should be addressed.
Received 1/27/87. Revised 5/11/87. Accepted 5/19/87.
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |