Spurgers Kevin B, Gold David L, Coombes Kevin R, Bohnenstiehl Nicole L, Mullins Brian, Meyn Raymond E, Logothetis Christopher J, McDonnell Timothy J
Department of Molecular Pathology, University of Texas M D Anderson Cancer Center, Houston, TX 77030, USA.
J Biol Chem. 2006 Sep 1;281(35):25134-42. doi: 10.1074/jbc.M513901200. Epub 2006 Jun 23.
Historically, most studies attribute p53 function to the transactivation of target genes. That p53 can selectively repress genes to affect a cellular response is less widely appreciated. Available evidence suggests that repression is important for p53-induced apoptosis and cell cycle arrest. To better establish the scope of p53-repressed target genes and the cellular processes they may affect, a global expression profiling strategy was used to identify p53-responsive genes following adenoviral p53 gene transfer (Ad-p53) in PC3 prostate cancer cells. A total of 111 genes, 0.77% of the 14,500 genes represented on the Affymetrix U133A microarray, were repressed more than 2-fold (p < or = 0.05). Validation of the array data, using reverse transcription-PCR of 20 randomly selected genes, yielded a confirmation rate of >95.5% for the complete data set. Functional over-representation analysis revealed that cell cycle regulatory genes exhibited a highly significant enrichment (p < or = 5 x 10(-28)) within the transrepressed targets. 41% of the repressed targets are cell cycle regulators. A subset of these genes exhibited repression following DNA damage, preceding cell cycle arrest, in LNCaP cells. The use of a p53 small interfering RNA strategy in LNCaP cells and the use of p53-null cell lines demonstrated that this repression is p53-dependent. These findings identify a set of genes not known previously to be down-regulated by p53 and indicate that p53-induced cell cycle arrest is a function of not only the transactivation of cell cycle inhibitors (e.g. p21) but also the repression of targets that regulate proliferation at several distinct phases of the cell cycle.
从历史角度看,大多数研究将p53的功能归因于其对靶基因的反式激活作用。p53能够选择性地抑制基因以影响细胞反应这一点,尚未得到广泛认识。现有证据表明,抑制作用对于p53诱导的细胞凋亡和细胞周期停滞很重要。为了更好地确定p53抑制的靶基因范围及其可能影响的细胞过程,采用了一种全基因组表达谱分析策略,以鉴定在PC3前列腺癌细胞中腺病毒p53基因转移(Ad-p53)后p53反应性基因。在Affymetrix U133A微阵列上所代表的14,500个基因中,共有111个基因(占0.77%)被抑制超过2倍(p≤0.05)。通过对20个随机选择的基因进行逆转录PCR来验证阵列数据,对整个数据集的确认率>95.5%。功能过表达分析表明,细胞周期调控基因在反式抑制的靶标中表现出高度显著的富集(p≤5×10-28)。41%的被抑制靶标是细胞周期调节因子。在LNCaP细胞中,这些基因的一个子集在DNA损伤后、细胞周期停滞之前表现出抑制作用。在LNCaP细胞中使用p53小干扰RNA策略以及使用p53缺失细胞系表明,这种抑制作用是p53依赖性的。这些发现确定了一组以前未知被p53下调的基因,并表明p53诱导的细胞周期停滞不仅是细胞周期抑制剂(如p21)反式激活的结果,也是在细胞周期几个不同阶段调节增殖的靶标受到抑制的结果。