Wild type p53 reactivation: From lab bench to clinic

被引：59
|
作者：
Selivanova, Galina [1 ]
机构：
[1] Karolinska Inst, Dept Microbiol Tumor & Cell Biol, SE-17177 Stockholm, Sweden
来源：
FEBS LETTERS | 2014年 / 588卷 / 16期
基金：
瑞典研究理事会;
关键词：
p53; Small molecule; Mdm2; MdmX; Apoptosis; ROS; SMALL-MOLECULE RITA; P53-MEDIATED TUMOR SUPPRESSION; UBIQUITIN LIGASE ACTIVITY; RNA-POLYMERASE I; CANCER-THERAPY; MUTANT P53; DNA-DAMAGE; EMBRYONIC LETHALITY; MDM2; INHIBITOR; GROWTH ARREST;
D O I：
10.1016/j.febslet.2014.03.049
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The p53 tumor suppressor is the most frequently inactivated gene in cancer. Several mouse models have demonstrated that the reconstitution of the p53 function suppresses the growth of established tumors. These facts, taken together, promote the idea of p53 reactivation as a strategy to combat cancer. This review will focus on recent advances in the development of small molecules which restore the function of wild type p53 by blocking its inhibitors Mdm2 and MdmX or their upstream regulators and discuss the impact of different p53 functions for tumor prevention and tumor eradication. Finally, the recent progress in p53 research will be analyzed concerning the role of p53 cofactors and cellular environment in the biological response upon p53 reactivation and how this can be applied in clinic. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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页码：2628 / 2638
页数：11
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