Bregman M D, Peters E, Sander D, Meyskens F L
J Natl Cancer Inst. 1983 Nov;71(5):927-32.
The cloning efficiencies of a murine melanoma cell line (S91 CCL 53.1) and a human melanoma cell strain (C8146c) were inhibited by dexamethasone (DEX), prostaglandin A1 (PGA1), and beta-all-trans-retinoic acid (RA) in a dose-dependent manner. Murine melanoma tumor colony-forming units (MTCFU) were inhibited more than 99% by DEX (1 X 10(-7) M) and RA (1 X 10(-7) M) with a concentration needed to produce a 50% reduction in colony formation for both hormones of 5 X 10(-9) M. Combinations of DEX and RA effected a synergistic inhibition on colony formation, which was reflected by a 11/2 log reduction in the hormone concentration needed to produce a greater than 99% inhibition of colony formation. When PGA1 was added to DEX and RA, a greater than additive reduction in colony formation was observed. Human MTCFU from cell strain C8146c were inhibited more than 85% at an RA concentration of 1 X 10(-7) M, but they were reduced only to 40% of control at a DEX concentration of 1 X 10(-6) M. DEX-RA produced an additive inhibition of colony formation. Addition of submaximal amounts of PGA1 to DEX-RA combinations or to either hormone alone resulted in synergistic reduction of human MTCFU. These results demonstrated that the proliferative potential of human and murine melanomas can be simultaneously regulated by DEX, PGA1, and RA.
地塞米松（DEX）、前列腺素A1（PGA1）和β-全反式维甲酸（RA）以剂量依赖方式抑制小鼠黑色素瘤细胞系（S91 CCL 53.1）和人黑色素瘤细胞株（C8146c）的克隆效率。DEX（1×10⁻⁷ M）和RA（1×10⁻⁷ M）对小鼠黑色素瘤肿瘤集落形成单位（MTCFU）的抑制率超过99%，两种激素产生50%集落形成减少所需的浓度均为5×10⁻⁹ M。DEX和RA联合对集落形成产生协同抑制作用，这表现为产生大于99%集落形成抑制所需的激素浓度降低1.5个对数。当将PGA1添加到DEX和RA中时，观察到集落形成的减少大于相加作用。来自细胞株C8146c的人MTCFU在RA浓度为1×10⁻⁷ M时抑制率超过85%，但在DEX浓度为1×10⁻⁶ M时仅降至对照的40%。DEX - RA对集落形成产生相加抑制作用。向DEX - RA组合或单独的任何一种激素中添加亚最大量的PGA1会导致人MTCFU的协同减少。这些结果表明，DEX、PGA1和RA可同时调节人和小鼠黑色素瘤的增殖潜能。
