摘要
端粒酶和p53两者在肿瘤和衰老的发生发展过程中都起着关键的作用。在人类大多数的肿瘤中都发现了这一现象:p53基因发生突变和端粒酶的重新激活。端粒酶和p53基因的治疗逐渐成为肿瘤治疗的重要手段之一。文章论述了端粒酶或p53基因敲除的不同组合的小鼠模型(mTR-/-p53+/+;mTR-/-P53-/-)的衰老与肿瘤表型,对端粒功能异常可抑制或促进肿瘤发生的辩证作用作一综述,以期理解p53与端粒酶在衰老与肿瘤发生中的辩证相互作用,寻求一种治疗肿瘤的新思路。
Telomerase and p53 play critical roles in tumorigenesis and senescence. The mutation of p53 gene and the reactivation of telomerase have been found in most of the human tumors. Aiming telomerase and p53 genes have become important strategies in tumor therapy. We reviewed the aging and tumor phenotype in different status of telomerase and p53 （mTR^-/-p53^＋/＋; mTR^-/-P53^-/-）, which indicated that telomere dysfunction could initiate or suppress the tumorigenesis depending on the status of p53. This helps further understanding of the crosstalk between p53 and telomerase in aging and tumorigenesis, and provides a new idea for treating tumor.
出处
《遗传》
CAS
CSCD
北大核心
2009年第5期451-456,共6页
Hereditas（Beijing)
基金
国家自然科学基金项目(编号:30771194)资助
关键词
端粒酶
P53
肿瘤
衰老
telomerase
p53
tumorigenesis
aging
