期刊
FRONTIERS IN ONCOLOGY
卷 10, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fonc.2020.595187
关键词
mutant p53 protein; gain-of-function; targeted therapy; tumorigenesis; drug resistance
类别
资金
- National Natural Science Foundation of China [91959204, 81930084, 815300045, 81871197, 81703092]
- leading talents of Guangdong Province Program [00201516]
- Shenzhen Sanming Project of Medicine [SZSM201602102]
- Development and Reform Commission of Shenzhen Municipality [S2016004730009]
TP53 is the most frequently mutated tumor suppressor gene in human cancer. The majority of mutations of p53 are missense mutations, leading to the expression of the full length p53 mutant proteins. Mutant p53 (Mutp53) proteins not only lose wild-type p53-dependent tumor suppressive functions, but also frequently acquire oncogenic gain-of-functions (GOF) that promote tumorigenesis. In this review, we summarize the recent advances in our understanding of the oncogenic GOF of mutp53 and the potential therapies targeting mutp53 in human cancers. In particular, we discuss the promising drugs that are currently under clinical trials as well as the emerging therapeutic strategies, including CRISPR/Cas9 based genome edition of mutant TP53 allele, small peptide mediated restoration of wild-type p53 function, and immunotherapies that directly eliminate mutp53 expressing tumor cells.
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