Mutant p53: One, no One, and One Hundred Thousand

被引:66
|
作者
Walerych, Dawid [1 ]
Lisek, Kamil [1 ,2 ]
Del Sal, Giannino [1 ,2 ]
机构
[1] Lab Nazl CIB, Trieste, Italy
[2] Univ Trieste, Dipartimento Sci Vita, Trieste, Italy
来源
FRONTIERS IN ONCOLOGY | 2015年 / 5卷
关键词
p53; mutation; gain-of-function; cancer; drug therapy; combination; oncogenes; tumor suppressor proteins; GAIN-OF-FUNCTION; LI-FRAUMENI-SYNDROME; NEGATIVE BREAST-CANCER; IN-VIVO; TUMOR-CELLS; CORE DOMAIN; MEVALONATE PATHWAY; GENE-EXPRESSION; INDUCE; REACTIVATION;
D O I
10.3389/fonc.2015.00289
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Encoded by the mutated variants of the TP53 tumor suppressor gene, mutant p53 proteins are getting an increased experimental support as active oncoproteins promoting tumor growth and metastasis. p53 missense mutant proteins are losing their wild-type tumor suppressor activity and acquire oncogenic potential, possessing diverse transforming abilities in cell and mouse models. Whether various mutant p53s differ in their oncogenic potential has been a matter of debate. Recent discoveries are starting to uncover the existence of mutant p53 downstream programs that are common to different mutant p53 variants. In this review, we discuss a number of studies on mutant p53, underlining the advantages and disadvantages of alternative experimental approaches that have been used to describe the numerous mutant p53 gain-of-function activities. Therapeutic possibilities are also discussed, taking into account targeting either individual or multiple mutant p53 proteins in human cancer.
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页数:7
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