Although cancers have altered glucose metabolism, termed the Warburg effect, 
which describes the increased uptake and conversion of glucose to lactate by 
cancer cells under adequate oxygen tension, changes in the metabolism of 
glutamine and fatty acid have also been documented. The MYC oncogene, which 
contributes to the genesis of many human cancers, encodes a transcription factor 
c-Myc, which links altered cellular metabolism to tumorigenesis. c-Myc regulates 
genes involved in the biogenesis of ribosomes and mitochondria, and regulation 
of glucose and glutamine metabolism. With E2F1, c-Myc induces genes involved in 
nucleotide metabolism and DNA replication, and microRNAs that homeostatically 
attenuate E2F1 expression. With the hypoxia inducible transcription factor 
HIF-1, ectopic c-Myc cooperatively induces a transcriptional program for hypoxic 
adaptation. Myc regulates gene expression either directly, such as glycolytic 
genes including lactate dehydrogenase A (LDHA), or indirectly, such as 
repression of microRNAs miR-23a/b to increase glutaminase (GLS) protein 
expression and glutamine metabolism. Ectopic MYC expression in cancers, 
therefore, could concurrently drive aerobic glycolysis and/or oxidative 
phosphorylation to provide sufficient energy and anabolic substrates for cell 
growth and proliferation in the context of the tumor microenvironment. 
Collectively, these studies indicate that Myc-mediated altered cancer cell 
energy metabolism could be translated for the development of new anticancer 
therapies.