It is well known that upon stress, the level of the tumor suppressor p53 is 
remarkably elevated. However, despite extensive studies, the underlying 
mechanism involving important inter-players for stress-induced p53 regulation is 
still not fully understood. We present evidence that the human lincRNA-RoR (RoR) 
is a strong negative regulator of p53. Unlike MDM2 that causes p53 degradation 
through the ubiquitin-proteasome pathway, RoR suppresses p53 translation through 
direct interaction with the heterogeneous nuclear ribonucleoprotein I (hnRNP I). 
Importantly, a 28-base RoR sequence carrying hnRNP I binding motifs is essential 
and sufficient for p53 repression. We further show that RoR inhibits 
p53-mediated cell cycle arrest and apoptosis. Finally, we demonstrate a RoR-p53 
autoregulatory feedback loop where p53 transcriptionally induces RoR expression. 
Together, these results suggest that the RoR-hnRNP I-p53 axis may constitute an 
additional surveillance network for the cell to better respond to various 
stresses.