糖皮质激素刺激B16黑色素瘤细胞中的黑色素生成和酪氨酸酶基因表达。
Glucocorticoid stimulates melanogenesis and tyrosinase gene expression in B16 melanoma cells.
作者信息
Ito A, Tanaka C, Takeuchi T, Mishima Y
机构信息
Department of Dermatology, Kobe University School of Medicine, Japan.
出版信息
Pigment Cell Res. 1991 Dec;4(5-6):247-51. doi: 10.1111/j.1600-0749.1991.tb00448.x.
Effects of dexamethasone on melanogenesis and tyrosinase mRNA levels were determined in B16/F10 melanoma cells. Melanin content of B16 cells increased in a dose-dependent manner by the addition of dexamethasone to the culture medium. After 72 hr exposure, dexamethasone (10(-6) M) produced a 2.4-fold increase in melanin content. Northern blot analysis revealed that tyrosinase mRNA level also increased by the addition of dexamethasone to the culture medium. After 24 hr exposure, dexamethasone (10(-6) M) caused a 1.8-fold increase in tyrosinase mRNA levels. A tumor promoter, 12-O-tetradecanoyl phorbol-13-acetate (TPA) decreased tyrosinase mRNA level at 30 nM concentration. Dexamethasone antagonized this TPA-mediated decrease in tyrosinase mRNA. It is suggested that glucocorticoids are involved in the regulation of tyrosinase activity at the transcriptional level.
在地塞米松对B16/F10黑色素瘤细胞黑色素生成及酪氨酸酶mRNA水平的影响研究中，向培养基中添加地塞米松后，B16细胞的黑色素含量呈剂量依赖性增加。暴露72小时后，地塞米松（10⁻⁶ M）使黑色素含量增加了2.4倍。Northern印迹分析显示，向培养基中添加地塞米松后，酪氨酸酶mRNA水平也升高。暴露24小时后，地塞米松（10⁻⁶ M）使酪氨酸酶mRNA水平增加了1.8倍。肿瘤促进剂12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯（TPA）在30 nM浓度时可降低酪氨酸酶mRNA水平。地塞米松可拮抗TPA介导的酪氨酸酶mRNA水平降低。提示糖皮质激素在转录水平参与酪氨酸酶活性的调节。
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