Tumor suppressor protein p53 plays a crucial role in maintaining genomic 
integrity in response to DNA damage. Regulation of translation of p53 mRNA is a 
major mode of regulation of p53 expression under genotoxic stress. The AU/U-rich 
element-binding protein HuR has been shown to bind to p53 mRNA 3'UTR and enhance 
translation in response to DNA-damaging UVC radiation. On the other hand, the 
microRNA miR-125b is reported to repress p53 expression and stress-induced 
apoptosis. Here, we show that UVC radiation causes an increase in miR-125b level 
in a biphasic manner, as well as nuclear cytoplasmic translocation of HuR. 
Binding of HuR to the p53 mRNA 3'UTR, especially at a site adjacent to the 
miR-125b target site, causes dissociation of the p53 mRNA from the RNA-induced 
silencing complex (RISC) and inhibits the miR-125b-mediated translation 
repression of p53. HuR prevents the oncogenic effect of miR-125b by reversing 
the decrease in apoptosis and increase in cell proliferation caused by the 
overexpression of miR-125b. The antagonistic interplay between miR-125b and HuR 
might play an important role in fine-tuning p53 gene expression at the 
post-transcriptional level, and thereby regulate the cellular response to 
genotoxic stress.