P63 and P73 Activation in Cancers with p53 Mutation

• Published in: Biomedicines Vol. 10; no. 7; p. 1490
• Main Authors: Cai, Bi-He, Hsu, Yun-Chien, Yeh, Fang-Yu, Lin, Yu-Rou, Lu, Rui-Yu, Yu, Si-Jie, Shaw, Jei-Fu, Wu, Ming-Han, Tsai, Yi-Zhen, Lin, Ying-Chen, Bai, Zhi-Yu, Shih, Yu-Chen, Hsu, Yi-Chiang, Liao, Ruo-Yu, Kuo, Wei-Hsin, Hsu, Chao-Tien, Lien, Ching-Feng, Chen, Chia-Chi
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 23.06.2022; MDPI
• Subjects: aggregation; Antitumor agents; Apoptosis; Binding sites; Cancer; Cancer therapies; Cell cycle; Cloning; Congenital diseases; Drugs; gain of function; Gene mutations; Genes; Genetic aspects; Health aspects; Heat shock proteins; Isoforms; Missense mutation; Mutants; Mutation; Mutation rates; Nonsense mutation; Ovaries; p53; p53 Protein; p63; p73; Review; Transcription factors; Tumor proteins; Tumor suppressor genes; Tumors; Taiwan
• ISSN: 2227-9059; 2227-9059
• DOI: 10.3390/biomedicines10071490

The members of the p53 family comprise p53, p63, and p73, and full-length isoforms of the p53 family have a tumor suppressor function. However, p53, but not p63 or p73, has a high mutation rate in cancers causing it to lose its tumor suppressor function. The top and second-most prevalent p53 mutations are missense and nonsense mutations, respectively. In this review, we discuss possible drug therapies for nonsense mutation and a missense mutation in p53. p63 and p73 activators may be able to replace mutant p53 and act as anti-cancer drugs. Herein, these p63 and p73 activators are summarized and how to improve these activator responses, particularly focusing on p53 gain-of-function mutants, is discussed.