The microRNA miR-504 targets TP53 mRNA encoding the p53 tumor suppressor. 
miR-504 resides within the fibroblast growth factor 13 (FGF13) gene, which is 
overexpressed in various cancers. We report that the FGF13 locus, comprising 
FGF13 and miR-504, is transcriptionally repressed by p53, defining an additional 
negative feedback loop in the p53 network. Furthermore, we show that FGF13 1A is 
a nucleolar protein that represses ribosomal RNA transcription and attenuates 
protein synthesis. Importantly, in cancer cells expressing high levels of FGF13, 
the depletion of FGF13 elicits increased proteostasis stress, associated with 
the accumulation of reactive oxygen species and apoptosis. Notably, stepwise 
neoplastic transformation is accompanied by a gradual increase in FGF13 
expression and increased dependence on FGF13 for survival ("nononcogene 
addiction"). Moreover, FGF13 overexpression enables cells to cope more 
effectively with the stress elicited by oncogenic Ras protein. We propose that, 
in cells in which activated oncogenes drive excessive protein synthesis, FGF13 
may favor survival by maintaining translation rates at a level compatible with 
the protein quality-control capacity of the cell. Thus, FGF13 may serve as an 
enabler, allowing cancer cells to evade proteostasis stress triggered by 
oncogene activation.