Chen Zujian, Liu Xiqiang, Wang Cheng, Jin Yi, Wang Yun, Wang Anxun, Zhou Xiaofeng
Center for Molecular Biology of Oral Diseases, College of Dentistry, University of Illinois at Chicago, Chicago, IL, USA.
Oncol Lett. 2011 Sep;2(5):919-922. doi: 10.3892/ol.2011.331.
Angiotensin II AT(2) receptor interacting protein 1 (ATIP1) has been recently identified as a tumor suppressor. In the present study, a 2.2 kb fragment of the 5' flanking region of the human ATIP1 gene was cloned, and its promoter activity was confirmed. Two putative p53 binding sites were identified in the minimal promoter. Cisplatin treatment and ectopic expression of p53 led to enhanced ATIP1 expression. Knockdown of p53 reduced the ATIP1 expression. The direct interaction of p53 and the ATIP1 promoter was confirmed by reporter gene and chromatin-immunoprecipitation assays. When the p53 sites were mutated, the effect of p53 on ATIP1 promoter was eliminated. The results suggest that the ATIP1 gene is regulated by p53 at the transcriptional level, and that it may play an important role in cancer initiation and progression.
血管紧张素II AT(2)受体相互作用蛋白1（ATIP1）最近被鉴定为一种肿瘤抑制因子。在本研究中，克隆了人ATIP1基因5'侧翼区的一个2.2 kb片段，并证实了其启动子活性。在最小启动子中鉴定出两个假定的p53结合位点。顺铂处理和p53的异位表达导致ATIP1表达增强。p53的敲低降低了ATIP1的表达。报告基因和染色质免疫沉淀试验证实了p53与ATIP1启动子的直接相互作用。当p53位点发生突变时，p53对ATIP1启动子的作用被消除。结果表明，ATIP1基因在转录水平上受p53调控，并且它可能在癌症的发生和发展中起重要作用。
