遗传 ›› 2009, Vol. 31 ›› Issue (5): 451-456.doi: 10.3724/SP.J.1005.2009.00451

• 综述 • 上一篇    下一篇

衰老或肿瘤: 端粒酶和p53的相互作用

张秀峰;唐文如;罗瑛   

  1. 昆明理工大学生命科学与技术学院 衰老与肿瘤分子遗传学实验室, 昆明 650224
  • 收稿日期:2008-09-22 修回日期:2008-11-07 出版日期:2009-05-10 发布日期:2009-05-10
  • 通讯作者: 罗瑛

Aging or tumor: the crosstalk between telomerase and p53

ZHANG Xiu-Feng;TANG Wen-Ru;LUO Ying   

  1. Lab of Molecular Genetics of Aging and Tumor, Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming 650224, China
  • Received:2008-09-22 Revised:2008-11-07 Online:2009-05-10 Published:2009-05-10
  • Contact: LUO Ying

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。

关键词: 肿瘤, 衰老, 端粒酶, p53

Abstract: Telomerase and p53 play critical roles in tumorigenesis and senescence. The mutation of p53 gene and the reac-tivation of telomerase have been found in most of the human tumors. Aiming telomerase and p53 genes have become im-portant 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 de-pending 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.