Fuse H, Akimoto S, Sato R, Miyauchi T, Wakisaka M, Hosoya T, Shimazaki J
Endocrinol Jpn. 1983 Apr;30(2):189-97. doi: 10.1507/endocrj1954.30.189.
The effect of testosterone treatment on the cytosolic androgen receptor in an androgen-dependent tumor (Shionogi Carcinoma 115, SC 115) and its sublines of altered hormone-dependency (CS 1, less androgen-dependent, and CS 2, androgen-independent) was examined. In all tumors examined a single, high-affinity binding to 3H-R 1881 was detected in cytosols. The size of the maximum binding sites was in the order SC 115, CS 1 and CS 2. Inhibition experiments revealed that the binding to 3H-R 1881 in cytosols of these tumors was attributable to the androgen receptor. The amount of the androgen receptor in cytosols was decreased at 1 hr after testosterone injection, then replenished gradually towards the pretreatment level. Depletion of the androgen receptor was dependent on the dose of testosterone administered. Multiple injections of testosterone depressed the replenishment of the receptor. Treatment with actinomycin D or cycloheximide did not alter the dynamics of the androgen receptor. Therefore, it was concluded that the depletion and replenishment of the androgen receptor in cytosols of the tumors were caused by receptor recycling. Because a similar pattern of depletion and replenishment of the androgen receptor was also observed in the less androgen-dependent tumors, the growth of tumors was felt to be unrelated to the receptor dynamics.
研究了睾酮治疗对雄激素依赖性肿瘤（Shionogi癌115，SC 115）及其激素依赖性改变的亚系（CS 1，雄激素依赖性较低；CS 2，雄激素非依赖性）胞质雄激素受体的影响。在所有检测的肿瘤中，胞质溶胶中均检测到与3H-R 1881的单一高亲和力结合。最大结合位点的大小顺序为SC 115、CS 1和CS 2。抑制实验表明，这些肿瘤胞质溶胶中与3H-R 1881的结合归因于雄激素受体。睾酮注射后1小时，胞质溶胶中雄激素受体的量减少，然后逐渐恢复到预处理水平。雄激素受体的耗竭取决于所给予的睾酮剂量。多次注射睾酮会抑制受体的恢复。用放线菌素D或环己酰亚胺处理不会改变雄激素受体的动态变化。因此，得出结论，肿瘤胞质溶胶中雄激素受体的耗竭和恢复是由受体循环引起的。由于在雄激素依赖性较低的肿瘤中也观察到了类似的雄激素受体耗竭和恢复模式，因此认为肿瘤的生长与受体动态变化无关。
