Tokino T, Nakamura Y
Laboratory of Molecular Medicine, Human Genome Center, The Institute of Medical Science, The University of Tokyo, Japan.
Crit Rev Oncol Hematol. 2000 Jan;33(1):1-6. doi: 10.1016/s1040-8428(99)00051-7.
The tumor suppressor gene p53 is mutated in a large proportion of human cancers. In some cellular conditions like DNA damage, the p53 gene is induced and its gene product is posttranscriptionally activated. p53 works as a transcriptional activator and induces the expression of its downstream target genes. This review will explain why expression of the normal p53 gene leads to tumor growth suppression. The p53 has several biological effects involving cell-cycle arrest, DNA replication and repair, proliferation, apoptosis, angiogenesis inhibition, and cellular stress response. These effects of the p53 result mainly from the activation of expression of a large number of p53-target genes. Here we have focused on the biological functions of the transcriptional targets of p53.
肿瘤抑制基因p53在很大一部分人类癌症中发生突变。在某些细胞状况下，如DNA损伤时，p53基因被诱导，其基因产物在转录后被激活。p53作为转录激活因子发挥作用，诱导其下游靶基因的表达。本综述将解释为何正常p53基因的表达会导致肿瘤生长抑制。p53具有多种生物学效应，包括细胞周期停滞、DNA复制与修复、增殖、凋亡、血管生成抑制以及细胞应激反应。p53的这些效应主要源于大量p53靶基因表达的激活。在此，我们重点关注p53转录靶点的生物学功能。
