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衰老或肿瘤: 端粒酶和p53的相互作用

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  • 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

  网络出版日期: 2009-05-10

Aging or tumor: the crosstalk between telomerase and p53

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  • Lab of Molecular Genetics of Aging and Tumor, Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming 650224, China

Received date: 2008-09-22

  Revised date: 2008-11-07

  Online published: 2009-05-10

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

本文引用格式

张秀峰,唐文如,罗瑛 . 衰老或肿瘤: 端粒酶和p53的相互作用[J]. 遗传, 2009 , 31(5) : 451 -456 . DOI: 10.3724/SP.J.1005.2009.00451

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.
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