Wolf D, Rotter V
Proc Natl Acad Sci U S A. 1985 Feb;82(3):790-4. doi: 10.1073/pnas.82.3.790.
The tumor antigen p53 is overproduced in transformed cells of various species, including man. HL-60 is an exceptional human tumor cell line that does not express this protein. Hybridization of polyadenylylated mRNA of these cells with a human p53 cDNA probe (p53-H14), which we cloned, had indicated a total absence of the mature-size (3.0 kilobases) or any aberrant p53 mRNA species. Analysis of the genomic HL-60 DNA indicated that the p53 gene in these cells was significantly altered. Most of the gene was deleted, and the residual p53 sequences of these cells, which show weak homology, mapped to the corresponding 5' region of the p53 gene. In agreement with previously documented results, we found that HL-60 cells have an amplified c-myc gene. We suggest that the deficiency of the p53 protein in HL-60 cells could have been overcome by using an alternative metabolic pathway. The c-myc product is a candidate for such an alternative protein.
肿瘤抗原p53在包括人类在内的各种物种的转化细胞中过度产生。HL-60是一种特殊的人类肿瘤细胞系，不表达这种蛋白质。这些细胞的多聚腺苷酸化mRNA与我们克隆的人p53 cDNA探针（p53-H14）杂交，表明完全不存在成熟大小（3.0千碱基）或任何异常的p53 mRNA种类。对HL-60基因组DNA的分析表明，这些细胞中的p53基因发生了显著改变。大部分基因被删除，这些细胞中残留的p53序列显示出微弱的同源性，定位于p53基因相应的5'区域。与先前记录的结果一致，我们发现HL-60细胞有一个扩增的c-myc基因。我们认为，HL-60细胞中p53蛋白的缺乏可以通过使用替代代谢途径来克服。c-myc产物是这种替代蛋白的一个候选者。
