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首页> 外文期刊>Molecular and Cellular Biology >Tumorigenicity of fibroblast lines expressing the adenovirus E1a, cellular p53, or normal c-myc genes.
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Tumorigenicity of fibroblast lines expressing the adenovirus E1a, cellular p53, or normal c-myc genes.

机译：表达腺病毒E1A，细胞P53或正常C-MYC基因的成纤维细胞线的肿瘤性。

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摘要

Cellular and viral oncogenes have been linked to the transformation of established cell lines in vitro, to the induction of tumors in vivo, and to the partial transformation or immortalization of primary cells. Based on the ability to cooperate with mutated ras oncogenes in the transformation of primary cells, the adenovirus E1a and cellular p53 genes have been assigned an immortalizing activity. It is demonstrated in this paper that the adenovirus type 5 E1a gene and simian virus 40 promoter-linked p53 cDNA are able to transform previously immortalized cells to a tumorigenic phenotype without a significant change in cell morphology. It is also shown that, when linked to a constitutive promoter, the normal mouse and human c-myc genes have the same transforming activity. Cells transformed by each of these oncogenes have an increased capacity to grow in the absence of growth factors and a limited anchorage-independent growth capability.
机译：细胞和病毒型癌基因已与体外成立的细胞系的转化有关，对体内肿瘤的诱导以及原代细胞的部分转化或永生化。基于在原发性细胞转化中与突变的RAS癌基因合作的能力，已分配腺病毒E1a和细胞p53基因的永生化活性。本文证明了腺病毒型5e1a基因和​​猿猴病毒40启动子连接的p53 cDNA能够将先前的永生化细胞转化为致瘤表型而没有细胞形态的显着变化。还表明，当与组成型启动子连接时，常规小鼠和人C-MYC基因具有相同的转化活性。由这些癌基因的每种细胞转化的细胞具有增加的能力，在没有生长因子和有限的锚定无关的生长能力中生长。

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