The MYC proto-oncogene is downstream of many growth-related signal transduction pathways that senses the cellular environment, such that the presence of growth factors and nutrients stimulates MYC expression, which in turn produces a transcriptional factor that amplifies the expression of a broad spectrum of genes involving metabolism, cell cycle, and cell death regulation. Acute deregulation of MYC presumably leads to metabolic imbalances that trigger cell cycle checkpoints, such as p53 or ARF, rendering the cells non-proliferative or dead. During tumor development, however, loss of checkpoints unleashes the ability of deregulated MYC to drive nutrient (glucose and glutamine) uptake, lipogenesis, nucleotide and protein synthesis for ribosomal biogenesis, and cell cycle progression. Deregulation of MYC causes cells to be addicted to nutrients to support a constitutive program of growth. Herein, we review how MYC regulates metabolism and how MYC addiction could be exploited to develop therapies that are directed at metabolic pathways.
|Original language||English (US)|
|Title of host publication||Tumor Cell Metabolism: Pathways, Regulation and Biology|
|Number of pages||22|
|ISBN (Print)||9783709118245, 9783709118238|
|State||Published - Jan 1 2015|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)