LAUSR

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. Since the p53 pathway is historically among the most targeted pathway for the development of anti-cancer therapeutics, we have also summarized some of the recent approaches and advances in reviving the anti-proliferative activities of wild-type p53. In this perspective, we provide an insight into understanding p53 as a prion-like protein and propose cancer to be recognized as amyloid or prion-like disease.