Liu Ze-Jun, Lu Xin, Zhang Yun, Zhong Shan, Gu Shou-Zhi, Zhang Xiao-Bing, Yang Xin, Xin Hai-Ming
Laboratory of International Cooperation, Southwest Hospital, Third Military Medical University, Chongqing 400038, PR China.
FEBS Lett. 2005 Mar 14;579(7):1587-90. doi: 10.1016/j.febslet.2005.01.069.
The p53 protein is one of the best-known tumour suppressors. Recently discovered ASPP1 and ASPP2 are specific activators of p53. To understand, if apoptosis-stimulating protein of p53 (ASPP) inactivation offers a selective advantage to tumors that have wild-type p53, we measured the mRNA expression of ASPP1 and ASPP2 in tumor cell lines retaining wide-type p53. In addition, the CpG island methylation status of ASPP1 gene and ASPP2 gene in the 5'-untranslated region was also investigated in order to understand the possible cause of abnormal expression of ASPP1 and ASPP2 in the tumor cell lines retaining wide-type p53. The data showed that mRNA expression of ASPP1 and ASPP2 is downregulated and CpG island tested is hypermethylated. These results indicated that ASPP CpG island aberrant methylation could be one molecular and genetic alteration in wild-type p53 tumours.
p53蛋白是最著名的肿瘤抑制因子之一。最近发现的ASPP1和ASPP2是p53的特异性激活剂。为了了解p53凋亡刺激蛋白(ASPP)失活是否为具有野生型p53的肿瘤提供了选择性优势,我们检测了保留野生型p53的肿瘤细胞系中ASPP1和ASPP2的mRNA表达。此外,还研究了5'-非翻译区ASPP1基因和ASPP2基因的CpG岛甲基化状态,以了解在保留野生型p53的肿瘤细胞系中ASPP1和ASPP2异常表达的可能原因。数据显示,ASPP1和ASPP2的mRNA表达下调,检测的CpG岛高度甲基化。这些结果表明,ASPP CpG岛异常甲基化可能是野生型p53肿瘤中的一种分子和基因改变。