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Expression of wild-type p53 is not compatible with continued growth of p53-negative tumor cells.

机译:野生型p53的表达与p53阴性肿瘤细胞的持续生长不相容。

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Inactivation of the cellular p53 gene is a common feature of Friend virus-induced murine erythroleukemia cell lines and may represent a necessary step in the progression of this disease. As well, frequent loss or mutation of p53 alleles in diverse human tumors is consistent with the view of p53 as a tumor suppressor gene. To examine the significance of p53 gene inactivation in tumorigenesis, we have attempted to express transfected wild-type p53 in three p53-negative tumor cell lines: murine DP16-1 Friend erythroleukemia cells, human K562 cells, and SKOV-3 cells. We found that aberrant p53 proteins, which differ from wild-type p53 by a single amino acid substitution, were expressed stably in these cells, whereas wild-type p53 expression was not tolerated. The inability of p53-negative tumor cell lines to support long-term expression of wild-type p53 protein is consistent with the view that p53 is a tumor suppressor gene.
机译:细胞p53基因的失活是Friend病毒诱导的鼠红白血病细胞系的共同特征,可能代表了该病发展的必要步骤。同样,在多种人类肿瘤中p53等位基因的频繁丢失或突变与p53作为抑癌基因的观点一致。为了检查p53基因失活在肿瘤发生中的重要性,我们尝试在三种p53阴性肿瘤细胞系中表达转染的野生型p53:鼠DP16-1 Friend红白血病细胞,人K562细胞和SKOV-3细胞。我们发现异常p53蛋白,在单个细胞中稳定表达与野生型p53不同,而野生型p53的表达是不能容忍的。 p53阴性肿瘤细胞系不能支持野生型p53蛋白的长期表达与p53是肿瘤抑制基因的观点是一致的。

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