Hypoxia-inducible factor (HIF)-1 is a master transcription factor, which 
up-regulates glycolysis, erythropoiesis, and angiogenesis under hypoxia. 
HIF-1alpha accumulates in normoxic tumor cells, leading to glycolysis under 
aerobic conditions. This phenomenon, known as the "Warburg effect," is caused by 
a yet unknown mechanism. Here we show that transformed cells that express 
constitutively active pp60(c-Src) (Src) express HIF-1alpha protein under 
normoxia, which results in the expression of multiple HIF-1alpha target genes. 
We show that this occurrence is due to an enhanced rate of HIF-1alpha protein 
synthesis and not due to reduced HIF-1alpha degradation. Furthermore, we show 
that the Src-induced increase in protein synthesis is due to the global increase 
in the rate of cap-dependent translation and does not involve inhibition of 
HIF-1alpha degradation.