Christman J K, Silagi S, Newcomb E W, Silverstein S C, Acs G
Proc Natl Acad Sci U S A. 1975 Jan;72(1):47-50. doi: 10.1073/pnas.72.1.47.
The decrease of tumorigenicity by mouse melanoma clone B559 after growth in the presence of 5-bromodeoxyuridine (BrdU) has been correlated with a decrease in detectable cellular plasminogen activator. Reduction of both activities occurs after one to two cell divisions in the presence of this thymidine analog and is virtually complete within three to four cell cycles. These changes are fully reversible; four to five cell divisions in the absence of BrdU are sufficient to allow both tumorigenicity and plasminogen activator levels to return to normal. These results support the hypotheses that (a) the expression of a cellular plasminogen activator is closely associated with the transformation of normal to malignant cells and that (b) the suppression of tumorigenicity by BrdU reflects the capacity of this base analog to inhibit the expression of specialized functions which accompany the malignant state.
小鼠黑色素瘤克隆B559在5-溴脱氧尿苷(BrdU)存在的情况下生长后致瘤性降低,这与可检测到的细胞纤溶酶原激活物减少有关。在这种胸苷类似物存在的情况下,经过一到两个细胞分裂,两种活性都会降低,并且在三到四个细胞周期内几乎完全消失。这些变化是完全可逆的;在没有BrdU的情况下进行四到五次细胞分裂足以使致瘤性和纤溶酶原激活物水平恢复正常。这些结果支持以下假设:(a)细胞纤溶酶原激活物的表达与正常细胞向恶性细胞的转化密切相关;(b)BrdU对致瘤性的抑制反映了这种碱基类似物抑制伴随恶性状态的特殊功能表达的能力。