An extended Myc network contributes to glucose homeostasis in cancer and diabetes.

@article{Peterson2011AnEM,
  title={An extended Myc network contributes to glucose homeostasis in cancer and diabetes.},
  author={Christopher W. Peterson and Donald E. Ayer},
  journal={Frontiers in bioscience},
  year={2011},
  volume={16},
  pages={
          2206-23
        }
}
The Myc network of transcription factors plays pleiotropic roles in normal and pathological cell function. The canonical Myc network controls how the essential nutrients glucose and glutamine are utilized inside cells. The Myc network carries out this function by upregulating glucose and glutamine transporters and key enzymes in the glycolytic or glutaminolytic pathways. The Myc network also coordinates cellular utilization of glucose and glutamine in biosynthetic pathways by directly… 

Figures from this paper

The MYC transcription factor network: balancing metabolism, proliferation and oncogenesis
TLDR
It is suggested that oncogenic activation of MYC and/or loss of a MYC antagonist, results in an imbalance in the activity of the network as a whole, leading to tumor initiation, progression and maintenance.
Interactions between Myc and MondoA transcription factors in metabolism and tumourigenesis
TLDR
A working model is presented to explain why c-Myc and MondoA function cooperatively in some cancers and antagonistically in others and the therapeutic response of BRAFV600E melanoma cells to vemurafenib requires downregulation of c- myc and HIF-1α and upregulation of Mondo a-TXNIP, and the subsequent reprogramming away from aerobic glycolysis.
Hepatic glucose sensing and integrative pathways in the liver
TLDR
The hepatic glucose-sensing system is a functional network of enzymes and transcription factors that is critical for the maintenance of energy homeostasis and systemic glycemia and elucidation of the components and functional roles may contribute to the future treatment of liver diseases associated with deregulated glucose sensors.
Myc and ChREBP transcription factors cooperatively regulate normal and neoplastic hepatocyte proliferation in mice
TLDR
The findings define the individual and cooperative proliferative, metabolic, and transcriptional roles for the “Extended Myc Network” under both normal and neoplastic conditions.
Coordination of nutrient availability and utilization by MAX- and MLX-centered transcription networks.
TLDR
How cells sense and respond transcriptionally to essential nutrients, including glucose and glutamine, and how MAX- and MLX-centered transcription networks contribute to metabolic homeostasis in normal and neoplastic cells are reviewed.
The Protective Role of the Carbohydrate Response Element Binding Protein in the Liver: The Metabolite Perspective
TLDR
The recent evidence that high fructose intake causes more severe hepatocyte damage in ChREBP-deficient models confirms the crucial protective role for ChRE BP in maintaining intracellular phosphate homeostasis.
Glucose Induces Protein Targeting to Glycogen in Hepatocytes by Fructose 2,6-Bisphosphate-Mediated Recruitment of MondoA to the Promoter
TLDR
It is demonstrated that elevated fructose 2,6-bisphosphate is essential for recruitment of MondoA to the PTG promoter, consistent with a mechanism for gene regulation to maintain intracellular phosphate homeostasis.
The glucose-sensing transcription factor MLX balances metabolism and stress to suppress apoptosis and maintain spermatogenesis
TLDR
In vivo and in vitro studies implicate MLX and other members of the proximal MYC network in regulation of metabolism and differentiation, as well as in suppression of intrinsic and extrinsic death signaling pathways in both spermatogenesis and male germ cell tumors (MGCTs).
Normal and Neoplastic Growth Suppression by the Extended Myc Network
TLDR
The functions of these “Extended Myc Network” members are discussed, with particular emphasis on their roles in suppressing normal and neoplastic growth.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 128 REFERENCES
Myc regulates a transcriptional program that stimulates mitochondrial glutaminolysis and leads to glutamine addiction
TLDR
It is reported that 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, resulting in the reprogramming of mitochondrial metabolism to depend on glutaminolysis to sustain cellular viability and TCA cycle anapleurosis.
c-Myc suppression of miR-23 enhances mitochondrial glutaminase and glutamine metabolism
TLDR
The c-Myc oncogenic transcription factor, which is known to regulate microRNAs and stimulate cell proliferation, transcriptionally represses miR-23a and miB-23b, resulting in greater expression of their target protein, mitochondrial glutaminase, in human P-493 B lymphoma cells and PC3 prostate cancer cells, which leads to upregulation of glutamine catabolism.
c-Myc suppression of miR-23 a / b enhances mitochondrial glutaminase expression and glutamine metabolism
TLDR
The c-Myc (hereafter referred to as Myc) oncogenic transcription factor, which is known to regulate microRNAs and stimulate cell proliferation, transcriptionally represses miR-23a and miB-23b, resulting in greater expression of their target protein, mitochondrial glutaminase, in human P-493 B lymphoma cells and PC3 prostate cancer cells.
The molecular determinants of de novo nucleotide biosynthesis in cancer cells.
c-Myc activates multiple metabolic networks to generate substrates for cell-cycle entry
TLDR
It is demonstrated that endogenous c-myc increased 13C labeling of ribose sugars, purines and amino acids, indicating partitioning of glucose carbons into C1/folate and pentose phosphate pathways, and increased tricarboxylic acid cycle turnover at the expense of anaplerotic flux.
The glucose-responsive transcription factor ChREBP contributes to glucose-dependent anabolic synthesis and cell proliferation
TLDR
It is demonstrated that the expression of ChREBP can be induced in response to mitogenic stimulation and that the induction of Ch REBP is required for efficient cell proliferation, and that suppression ofChREBP led to a p53-dependent reduction in tumor growth.
Glutamine-dependent anapleurosis dictates glucose uptake and cell growth by regulating MondoA transcriptional activity
TLDR
Glucose-dependent mitochondrial anapleurosis dictates glucose uptake and aerobic glycolysis by blocking MondoA:Mlx-dependent transcriptional activation of TXNIP, proposing a metabolic checkpoint that restricts cell growth when subthreshold levels of these essential nutrients are available.
c-Myc Is Required for the Glucose-mediated Induction of Metabolic Enzyme Genes*
TLDR
It is concluded that multiple mechanisms exist to communicate the glucose-derived signal and that c-Myc has a key role in the hepatic glucose signaling pathway.
Glucose Controls Nuclear Accumulation, Promoter Binding, and Transcriptional Activity of the MondoA-Mlx Heterodimer
TLDR
The experiments establish the mechanistic circuitry by which cells sense and respond transcriptionally to various intracellular glucose levels and show that glucose is required at two additional steps to stimulate the transcription activation function of MondoA-Mlx complexes.
Q's next: the diverse functions of glutamine in metabolism, cell biology and cancer
TLDR
The protean roles of glutamine in cancer are reviewed, both in the direct support of tumor growth and in mediating some of the complex effects on whole-body metabolism that are characteristic of tumor progression.
...
1
2
3
4
5
...