Transformation of NIH/3T3 to anchorage independence by H-ras is accompanied by loss of suppressor activity.
Transformation of NIH/3T3 to anchorage independence by H-ras is accompanied by loss of suppressor activity.
复制标题
H-ras 将 NIH/3T3 转化为锚定独立性，并伴有抑制活性的丧失。
DOI：
10.1006/excr.1993.1081
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发表时间：
1993
影响因子：
3.7
通讯作者：
Bouck,NP
中科院分区：
文献类型：
--
作者：
Tolsma,SS;Cohen,JD;Ehrlich,LS;Bouck,NP
尽管NIH/3T3细胞对显性作用癌基因的转化非常敏感，但它们携带着抑制物。当细胞融合测试时，它们能够抑制由活化的H-Rasor N-ras转化的小鼠和人类细胞的锚定非依赖性表型。经苯甲酰胺处理的Ras转化NIH/3T3克隆的癌基因恢复为未转化的表型，但失去了抑制其他转化子的能力，表明它们的初始转化伴随着抑制子的丢失。在仓鼠细胞中，一种活性致癌基因使染色体分离率提高了100倍。这些结果表明，在体外转化NIH/3T3细胞中，ras可能比先前推测的更类似于多步骤活体肿瘤的发展，不仅涉及到活性癌基因的表达，而且涉及到抑制活性的丧失，可能是由裂解癌基因诱导的。
Despite their familiar sensitivity to transformation by dominant-actingrasoncogenes, NIH/3T3 cells carry arassuppressor. When tested by cell fusion they were able to suppress the anchorage-independent phenotype of both mouse and human cells transformed by activated H-rasor N-ras. This suppression occurred without a decrease in expression of the activatedrasoncogene.Ras-transformed NIH/3T3 clones cured of their oncogene by benzamide treatment reverted to a non-transformed phenotype, but had lost the ability to suppress otherrastransformants, indicating that their initial transformation was accompanied by suppressor loss. In hamster cells an activerasoncogene increased the rate of chromosome segregation by >100-fold. These results suggest thatin vitrotransformation of NIH/3T3 cells byrasmay be more similar to multistepin vivotumor development than previously suspected, involving not only expression of an active oncogene but also loss of a suppressor activity, perhaps induced by the clastogenic oncogene.