Fukuchi K, Tomoyasu S, Watanabe H, Kaetsu S, Tsuruoka N, Gomi K
Department of Clinical Pathology, Showa University, Tokyo, Japan.
Biol Chem Hoppe Seyler. 1995 Oct;376(10):627-30. doi: 10.1515/bchm3.1995.376.10.627.
Deferoxamine (DFO)-induced iron deprivation caused an increase in p53 expression in ML-1 and Raji cells. In ML-1 cells, with express wild type p53, p53 protein levels were transiently increased 6 h after addition of 10(-4)M DFO. In Raji cells, which carry a mutant p53 allele, p53 increased 6 h after addition of 10(-4)M DFO and remained elevated for 24 h. Growth inhibition was observed in both cell types 6 h after addition of 10(-4)M DFO. In both cells, p53 mRNA levels did not increase following incubation with DFO, suggesting that increased p53 expression is the result of a post-transcriptional mechanism. Although increases in wild type p53 protein in ML-1 cells resulted in increases in a p53 target gene, p21cipl/wafl/sdil, this effect was not observed in Raji cells which express a mutant p53 protein.
去铁胺（DFO）诱导的铁缺乏导致ML-1和Raji细胞中p53表达增加。在表达野生型p53的ML-1细胞中，加入10⁻⁴M DFO后6小时，p53蛋白水平短暂升高。在携带突变p53等位基因的Raji细胞中，加入10⁻⁴M DFO后6小时p53升高，并持续升高24小时。加入10⁻⁴M DFO后6小时，两种细胞类型均观察到生长抑制。在两种细胞中，与DFO孵育后p53 mRNA水平未增加，表明p53表达增加是转录后机制的结果。尽管ML-1细胞中野生型p53蛋白的增加导致p53靶基因p21cipl/wafl/sdil增加，但在表达突变p53蛋白的Raji细胞中未观察到这种效应。
