Abstract：
:The global transcription factor, p53, is a master regulator of gene expression in cells. Mutations in the TP53 gene promote unregulated cell growth through the inactivation of downstream effectors of the p53 pathway. In fact, mutant p53 is highly prone to misfolding and frequently resides inside the cell as large aggregates, causing loss of physiological function of the tumor-suppressor protein. Here, we review the plausible reasons for functional loss of p53, including amyloid formation leading to unhindered cancer progression. We discuss previous as well as recent findings regarding the amyloid formation of p53 in vitro and in vivo. We elaborate on prion-like properties of p53 amyloids and their possible involvement in cancer progression. Because the p53 pathway is historically most targeted for the development of anticancer therapeutics, we have also summarized some of the recent approaches and advances in reviving the antiproliferative activities of wild-type p53. In this Perspective, we provide insight into understanding p53 as a prion-like protein and propose cancer to be recognized as an amyloid or prion-like disease.
journal_name
Biochemistryjournal_title
Biochemistryauthors
Navalkar A,Ghosh S,Pandey S,Paul A,Datta D,Maji SKdoi
10.1021/acs.biochem.9b00796subject
Has Abstractpub_date
2020-01-21 00:00:00pages
146-155issue
2eissn
0006-2960issn
1520-4995journal_volume
59pub_type
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