Your browser doesn't support javascript.
loading
Effect of androgen on proliferation of estrogen-responsive transformed mouse Leydig cells in serum-free culture.
Nishizawa, Y; Sato, B; Nishii, K; Kishimoto, S; Matsumoto, K.
Afiliação
  • Nishizawa Y; Third Department of Internal Medicine, Osaka University Hospital, Japan.
Cancer Res ; 49(6): 1377-82, 1989 Mar 15.
Article em En | MEDLINE | ID: mdl-2924294
ABSTRACT
We examined the effects of steroid hormones on the proliferation of transformed mouse Leydig cells (B-1) in serum-free culture condition. Among hormones examined, androgen as well as estrogen enhanced the cell proliferation rate. Hormone binding studies revealed that B-1 cells contained both androgen and estrogen receptors. In addition, androgen-enhanced cell growth was inhibited by antiandrogen, but not by antiestrogen, while estrogen-stimulated cell growth was suppressed by antiestrogen. However, the simultaneous addition of androgen and estrogen did not show an additive effect. Dose-response study on androgen-dependent cell growth revealed that relatively high concentrations (10(-7)-10(-6) M) of dihydrotestosterone were required to obtain the maximum response. This was at least partly explained by the finding that B-1 cells could metabolize dihydrotestosterone into the less active steroids. Finally, B-1 cells were found to grow more rapidly in normal than in castrated male mice. These results clearly indicate that the proliferation of B-1 cells is stimulated by both androgen and estrogen, which utilize the different receptor systems.
Assuntos
Buscar no Google
Base de dados: MEDLINE Assunto principal: Neoplasias Testiculares / Estrogênios / Androgênios / Tumor de Células de Leydig / Neoplasias Hormônio-Dependentes Limite: Animals Idioma: En Ano de publicação: 1989 Tipo de documento: Article
Buscar no Google
Base de dados: MEDLINE Assunto principal: Neoplasias Testiculares / Estrogênios / Androgênios / Tumor de Células de Leydig / Neoplasias Hormônio-Dependentes Limite: Animals Idioma: En Ano de publicação: 1989 Tipo de documento: Article