PRMT5-dependent p53 escape in tumorigenesis

Abstract

Extensive studies have characterized mutational disruption of p53 signaling in human cancers. However, the mechanism for bypass of p53 function in tumors retaining wild-type p53 has remained ambiguous. Recent studies suggest that PRMT5, which is frequently elevated in human cancers, cooperates with oncogenic cyclin D1 and leaves marks on p53 by way of arginine methylation, promoting the bypass of wild-type p53, and in doing so, evade apoptosis.