Tomita Y, Kuwata T
Cancer Res. 1976 Sep;36(9 pt.1):3016-9.
Adriamycin inhibited the endogenous RNA-, poly (A)-d(T)12-, and calf thymus DNA-catalyzed reaction of reverse transcriptase from AKR mouse murine leukemia virus (AKR-MLV). This inhibition was found at the reaction levels of endogenous RNA-directed and subsequent DNA-directed DNA synthesis. Although adriamycin and actinomycin D significantly reduced the growth of AKR mouse cells (K3b), the treatment with adriamycin could bot inhibit the AKR-MLV production in these cells. Actinomycin D inhibited AKR-MLV production completely in the same experimental condition. In adriamycin-resistant K3b/Am cells, which were isolated by intermittent treatment of K3b cells with adriamycin, persistence of AKR-MLV was demonstrated. K3b/Am cells showed some altered characteristics such as reduced growth rate and tumorigenicity.
阿霉素抑制了来自AKR小鼠白血病病毒(AKR-MLV)的逆转录酶的内源性RNA、聚(A)-d(T)12以及小牛胸腺DNA催化的反应。在内源性RNA指导的以及随后的DNA指导的DNA合成反应水平上发现了这种抑制作用。尽管阿霉素和放线菌素D显著降低了AKR小鼠细胞(K3b)的生长,但用阿霉素处理并不能抑制这些细胞中AKR-MLV的产生。在相同实验条件下,放线菌素D完全抑制了AKR-MLV的产生。在用阿霉素间歇处理K3b细胞分离得到的阿霉素抗性K3b/Am细胞中,证实了AKR-MLV的持续存在。K3b/Am细胞表现出一些改变的特征,如生长速率降低和致瘤性降低。