Eliyahu D, Michalovitz D, Oren M
Nature. 1985;316(6024):158-60. doi: 10.1038/316158a0.
The p53 cellular tumour antigen, long known to be overproduced in a variety of neoplastically transformed cells, was recently shown to be directly involved in transformation. Thus, p53 can complement activated Ha-ras in transforming secondary rat embryo fibroblasts into grossly altered, tumorigenic cells. Moreover, p53 can also be shown to possess immortalizing activity. Our previous results indicated, however, that the contribution of p53 to the transformation was not synonymous with immortalization, suggesting that the two activities of the protein are probably separable. We demonstrate here that this is indeed the case, as overproduction of p53 in an established cell line, while not causing gross morphological changes, endows these cells with an overt tumorigenic potential. Furthermore, the tumorigenic efficiency of such cell lines may be correlated with the extent of p53 over-production.
p53细胞肿瘤抗原长期以来已知在多种肿瘤转化细胞中过量产生，最近研究表明它直接参与细胞转化。因此，p53在将原代大鼠胚胎成纤维细胞转化为明显改变的致瘤细胞过程中可补充激活的Ha-ras的作用。此外，p53也具有永生化活性。然而，我们之前的结果表明，p53对转化的作用并不等同于永生化，这表明该蛋白的这两种活性可能是可分离的。我们在此证明确实如此，因为在一个已建立的细胞系中过量表达p53，虽然不会引起明显的形态学变化，但赋予这些细胞明显的致瘤潜能。此外，此类细胞系的致瘤效率可能与p53过量表达的程度相关。
