Document Type

Article

Publication Date

2-2024

Identifier

DOI: 10.1016/j.nano.2024.102732

Abstract

Among the tumor suppressor genes, TP53 is the most frequently mutated in human cancers, and most mutations are missense mutations causing production of mutant p53 (mutp53) proteins. TP53 mutations not only results in loss of function (LOH) as a transcription factor and a tumor suppressor, but also gain wild-type p53 (WTp53)-independent oncogenic functions that enhance cancer metastasis and progression (Yamamoto and Iwakuma, 2018; Zhang et al., 2022). TP53 has extensively been studied as a therapeutic target as well as for drug development and therapies, however with limited success. Achieving targeted therapies for restoration of WTp53 function and depletion or repair of mutant p53 (mutp53) will have far reaching implication in cancer treatment and therapies. This review briefly discusses the role of p53 mutation in cancer and the therapeutic potential of restoring WTp53 through the advances in mRNA nanomedicine.

Journal Title

Nanomedicine

Volume

56

First Page

102732

Last Page

102732

MeSH Keywords

Humans; Tumor Suppressor Protein p53; RNA, Messenger; Neoplasms; Mutation; Transcription Factors; Cell Line, Tumor

Keywords

Gene therapy; Nanotechnology; Restoring wild-type p53; cancer; p53 mutant

Comments

This is an open access article distributed under the terms of the Creative Commons CC-BY license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Publisher's Link: https://www.sciencedirect.com/science/article/pii/S1549963424000017?via%3Dihub

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