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.