Cehovic G, Redding T W, Schally A V
Med Oncol Tumor Pharmacother. 1985;2(4):243-7. doi: 10.1007/BF02934909.
We studied endogenous phosphorylation in rat transplantable MT/W9A hormone-dependent mammary tumors of untreated rats and of animals treated with LH-RH analogs, the agonist D-Trp-6-LH-RH and the antagonist N-Ac-D-p-Cl-Phe1,2,D-Trp3,D-Arg6,D-Ala10-LH-RH. Incorporation of 32P from 32P-ATP was reduced significantly in tumors of rats treated with agonistic and antagonistic analogs of LH-RH or ovariectomized. The inhibition of protein phosphorylation may be related to tumor regression.
我们研究了未处理大鼠以及用促黄体生成素释放激素(LH-RH)类似物、激动剂D-色氨酸-6-LH-RH和拮抗剂N-乙酰-D-对氯苯丙氨酸1,2、D-色氨酸3、D-精氨酸6、D-丙氨酸10-LH-RH处理的动物的可移植性MT/W9A激素依赖性大鼠乳腺肿瘤中的内源性磷酸化。在用LH-RH激动剂和拮抗剂类似物处理或卵巢切除的大鼠肿瘤中,来自32P-ATP的32P掺入显著减少。蛋白质磷酸化的抑制可能与肿瘤消退有关。