Dees C, Travis C C
Health Sciences Research Division, Oak Ridge National Laboratory, TN 37831-6109, USA.
Cancer Lett. 1995 Sep 25;96(2):225-31. doi: 10.1016/0304-3835(95)03936-q.
Chemotherapeutic and DNA-damaging agents were found to increase p53 site-specific DNA binding in human breast and rat liver epithelial WBrasII cells which produce mutant p53. Increased p53 site-specific DNA binding by chemotherapeutic or DNA-damaging agents was also induced in transfected Saos-2 cells producing wild type or transforming mutant p53. Therefore, exposure of cells containing a transforming p53 mutant to chemotherapeutic or DNA-damaging agents may potentially enhance their transformation state and tumorigenic potential.
在产生突变型p53的人乳腺癌和大鼠肝上皮WBrasII细胞中，发现化疗药物和DNA损伤剂可增加p53位点特异性DNA结合。在产生野生型或转化突变型p53的转染Saos-2细胞中，化疗药物或DNA损伤剂也可诱导p53位点特异性DNA结合增加。因此，含有转化型p53突变体的细胞暴露于化疗药物或DNA损伤剂可能会潜在地增强其转化状态和致瘤潜力。
