Suzuki N, Miyauchi T, Urata M, Yazawa H, Shimazaki J, Hosoya T
Endocrinol Jpn. 1986 Apr;33(2):233-8. doi: 10.1507/endocrj1954.33.233.
The activity of ornithine decarboxylase in androgen-dependent mouse mammary tumor (Shionogi Carcinoma 115) was reduced to 25% by castration of tumor-bearing mice and restored to the normal level 12 h after administration of testosterone or 5 alpha-dihydrotestosterone. Administration of estradiol-17 beta to the tumor-bearing castrated mice also stimulated the enzyme activity while progesterone and cortisol had little effect. On the other hand, the enzyme activity was affected by neither castration nor androgen injection to CS 2, which is a subline of SC 115 and completely independent of androgen for growth. The inhibition of ornithine decarboxylase activity in SC 115 by injecting alpha-difluoromethylornithine did not affect the enhancement of RNA polymerase I activity by androgen, showing independent elevation of the levels of the two enzymes by androgen.
通过切除荷瘤小鼠的睾丸,雄激素依赖性小鼠乳腺肿瘤(Shionogi癌115)中的鸟氨酸脱羧酶活性降低至25%,在给予睾酮或5α-二氢睾酮12小时后恢复到正常水平。给切除睾丸的荷瘤小鼠注射17β-雌二醇也能刺激该酶的活性,而孕酮和皮质醇的影响很小。另一方面,CS 2(SC 115的一个亚系,其生长完全不依赖雄激素)的酶活性既不受去势影响,也不受雄激素注射的影响。通过注射α-二氟甲基鸟氨酸抑制SC 115中的鸟氨酸脱羧酶活性,并不影响雄激素对RNA聚合酶I活性的增强作用,表明雄激素可使这两种酶的水平独立升高。