abstract

• The p53 roles have been largely described; among them, cell proliferation and apoptosis control are some of the best studied and understood. Interestingly, the mutations on the six hotspot sites within the region that encodes the DNA-binding domain of p53 give rise to other very different variants. The particular behavior of these variants led to consider p53 mutants as separate oncogene entities; that is, they do not retain wild type functions but acquire new ones, namely Gain-of-function p53 mutants. Furthermore, recent studies have revealed how p53 mutants regulate gene expression and exert oncogenic effects by unbalancing specific microRNAs (miRNAs) levels that provoke epithelial-mesenchymal transition, chemoresistance, and cell survival, among others. In this review, we discuss recent evidence of the crosstalk between miRNAs and mutants of p53, as well as the consequent cellular processes dysregulated. Copyright © 2021 Madrigal, Hernández-Monge, Herrera, González-De la Rosa, Domínguez-Gómez, Candelaria, Luna-Maldonado, Calderón González and Díaz-Chávez.

authors

• Calderón-González K.G.
• Hernández Monge Jesús

publication date

• 2021-01-01

funding provided via

• Consejo Nacional de Ciencia y Tecnología, CONACYT: 168896, 261875  Grant

published in

• Frontiers in Cell and Developmental Biology  Journal

keywords

• cancer; gain of function; miRNA biogenesis; miRNAs; mutant p53

Digital Object Identifier (DOI)

• 10.3389/fcell.2021.695723

PubMed ID

start page

end page

volume

• 9

issue