Question

The Myc oncogene enhances anaplerotic glutamine utilization and as a consequence becomes dependent on exogenous supplied glutamine.

True or Flase

Answer 1

This statement is true because MYC regulates a transcriptional program that stimulates mitochondrial gluraminolysis and leads to glutamine addiction. Cells fuel their growth and proliferation through the catabolism of two main substrates: glucose and glutamine. Most of the remaining metabolites taken up by proliferating cells are not catabolised , but instead are used as building blocks during anabolic macromolecular synthesis. These oncogenes play a direct role in stimulating glucose uptake and metabolism, rendering the transformed cell addicted to glucose for the maintenance of survival. The transcriptional regulatory properties of the oncogene MYC coordinate the expression of genes necessary for cells to engage in glutamine catabolism that exceeds the cellular requirement for protein and nucleotide biosynthesis. A consequence of these MYC dependent glutaminolysis is the reprogramming of mitochondrial metabolism to depend on glutamine catabolism to sustain cellular viability. The ability of MYC expressing cells to engage in gluraminolysis does not depend on oncomitant activation.

The oncogenic levels of MYC induce a transcription program that promotes gluraminolysis and triggers cellular addiction to glutamine as a bio-energetic substrate.