Abstract��Abstract: The tumor suppressor p53 functions mainly as a transcription factor. It accumulates in cells and becomes activated in response to various cellular stresses such as hypoxia or DNA damage. Upon activation, p53 regulates the transcription of a series of genes, resulting in cell cycle arrest, apoptosis or senescence to prevent tumorigenesis. Dysfunction of p53 often leads to cancer. Mutation of the TP53 gene that encodes p53 protein is the main way of inactivating p53. Mutant p53 not only loses the tumor suppressive activity, but also gains dominant negative effect and new oncogenic property. Additionally, the function of wild-type p53 is regulated by its interacting proteins or non-coding RNA. Down-regulation of its positive regulators or/and up-regulation of its negative regulators can also inactivate wild-type p53. p53 is an important drug target. Many studies have demonstrated that cancer can be treated through restoring the normal function of mutant p53, degrading it, or enhancing the stability and activity of the wild-type protein. Based on the analysis of public cancer database and protein-protein interaction database, the influences of TP53 mutation, p53-in-teracting partners and non-coding RNA on p53 function are summarized, and the current status of the de-velopment of p53-targeted drugs is also introduced, which may be helpful for p53 and related drug research.
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�ܽ���. ��֢��p53ʧ��ķ��ӻ��ƺͰ���p53�Ŀ���ҩ���о���չ[J]. ������ѧ�о�, 2021, 25(3): 189-196. ZHOU Jian-lin. Research Progress on Molecular Mechanism of p53 Inactivation in Cancers and Drugs Targeting p53. Life Science Research, 2021, 25(3): 189-196.
