MicroRNAs and the Warburg effect: New players in an old arena

It is known that tumor cells adapt characteristic metabolic phenotypes during cancer initiation and progression. The hallmark of tumor metabolism is aerobic glycolysis, or Warburg Effect, which was first described more than 80 years ago. Unlike normal cells, most cancer cells produce energy by a high rate of glycolic catabolism to lactate in the cytosol, rather than by oxidation of pyruvate in mitochondria, even in the presence of oxygen. Progress over the past decade has revealed that alterations of oncogenes and tumor suppressors are responsible for such metabolic reprogramming in cancer cells, however, the underlying molecular basis remains largely unknown. Mounting evidence shows the interplay between microRNAs and oncogenes/tumor suppressors, via key metabolic enzyme effecters, which could facilitate the Warburg Effect in cancer cells. In this review, we will summarize our current understanding of the roles of microRNAs, in particular their interplay with oncogenes/tumor suppressors such as cMyc, HIF-1 and P53, in tumor metabolism.