WT1 inhibits AML cell proliferation in a p53-dependent manner.

ABSTRACT: WT1 has been reported to function as an oncogene and a tumor suppressor in acute myeloid leukemia (AML). The molecular mechanisms have not yet been fully elucidated. Here, we report that p53, served as a tumor suppressor, plays a critical role in regulating the function of WT1 in AML. For details, we performed a meta-analysis on 1131 AML cases, showing that WT1 gene mutation and TP53 gene exhibited a mutually exclusive predisposition in AML. p53 can be recruited to the promoter region of WT1's target genes to modulate their expression by physically interacting with WT1. The AML-derived p53 mutation (p53^R248Q) can disrupt the interaction between WT1 and p53, resulting in the loss of modulation of WT1's target genes. Furthermore, wild-type p53 maintained the anti-proliferation act

SUBMITTER: Yao Y 

PROVIDER: S-EPMC8409780 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature