Yoon Kyong-Ah, Nakamura Yusuke, Arakawa Hirofumi
Human Genome Center, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
Cancer Medicine and Biophysics Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.
J Hum Genet. 2004;49(3):134-140. doi: 10.1007/s10038-003-0122-3. Epub 2004 Feb 25.
To identify additional targets of p53, we used a cDNA microarray system to examine gene-expression patterns in response to enforced expression of exogenous p53 in p53-deficient cancer cells, and identified the aldehyde dehydrogenase 4 ( ALDH4) gene as a direct target of p53. ALDH4 is a mitochondrial-matrix NAD+-dependent enzyme catalyzing the second step of the proline degradation pathway. Expression of ALDH4 mRNA was induced in HCT116 cells in response to DNA damage caused by adriamycin treatment, in a p53-dependent manner. ALDH4 contains a potential p53 binding sequence in intron1 and the interaction of p53 with the site was shown by EMSA and ChIP assays. We confirmed p53-dependent transcriptional activity of the binding site by means of a reporter assay. Inhibition of ALDH4 expression by antisense oligonucleotides was able to enhance cell death induced by infection with Ad-p53. H1299 cells transformed to over-express ALDH4 showed significantly lower intracellular reactive oxygen species (ROS) levels than parental or control cells after treatment with hydrogen peroxide or UV. Those cells were also resistant to cell damage caused by hydrogen peroxide. These results suggest that p53 might play a protective role against cell damage induced by generation of intracellular ROS, through transcriptional activation of ALDH4.
为了鉴定p53的其他靶点,我们使用cDNA微阵列系统检测p53缺陷癌细胞中外源p53强制表达后的基因表达模式,并鉴定醛脱氢酶4(ALDH4)基因为p53的直接靶点。ALDH4是一种线粒体基质中依赖NAD+的酶,催化脯氨酸降解途径的第二步。阿霉素处理导致DNA损伤后,HCT116细胞中ALDH4 mRNA的表达以p53依赖的方式被诱导。ALDH4的内含子1中含有一个潜在的p53结合序列,电泳迁移率变动分析(EMSA)和染色质免疫沉淀分析(ChIP)显示p53与该位点存在相互作用。我们通过报告基因检测证实了该结合位点的p53依赖的转录活性。反义寡核苷酸抑制ALDH4表达能够增强Ad-p53感染诱导的细胞死亡。用过氧化氢或紫外线处理后,转化为过表达ALDH4的H1299细胞显示出比亲本细胞或对照细胞显著更低的细胞内活性氧(ROS)水平。这些细胞对过氧化氢引起的细胞损伤也具有抗性。这些结果表明,p53可能通过转录激活ALDH4对细胞内ROS产生诱导的细胞损伤发挥保护作用。