Myc regulates a transcriptional program that stimulates mitochondrial glutaminolysis and leads to glutamine addiction

By David R. Wise, Ralph J. Deberardinis, A. Mancuso, Nabil Sayed, Xiao-yong Zhang, H. Pfeiffer, Ilana B. Nissim, E. Daikhin, M. Yudkoff, S. McMahon and 1 more. Proceedings of the National Academy of Sciences of the United States of America, 2008

1,960 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/afd2e606ad8af9d3297ca7120c9025e7f7d15f6e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. C. V. Dang
2. M. V. Vander Heiden
3. Navdeep S. Chandel
4. Ralph J. Deberardinis
5. Craig B. Thompson
6. G. Semenza
7. Jie Zheng
8. David M. Sabatini

In Molecular Biology

1. C. V. Dang
2. M. V. Vander Heiden
3. Navdeep S. Chandel
4. Ralph J. Deberardinis
5. David M. Sabatini
6. Craig B. Thompson
7. G. Semenza
8. Jie Zheng

Citations in the corpus

• Tumour hypoxia induces a metabolic shift causing acidosis: a common feature in cancer (2009, background): “Myc not only regulates glucose metabolism but also activates glutaminolysis, as demonstrated recently [79].”
• Glutaminolysis and Transferrin Regulate Ferroptosis (2015, background): “We found that amino-oxyacetate (AOA), a pan inhibitor of transaminases (Wise et al., 2008), could inhibit serum-dependent necrosis but not TNFα-induced apoptosis in MEFs (Figure 5B and Figure S5E).”
• Mitochondrial metabolism and ROS generation are essential for Kras-mediated tumorigenicity (2010, background): “Previous studies indicate that cells overexpressing Myc utilize glutamine metabolism for their proliferation (13, 14).”
• Targeting lactate metabolism for cancer therapeutics. (2013, background): “In addition, MYC augments glutamine catabolism by inducing the transcription of the glutamine transporter ASC-like Na+-dependent neutral amino acid transporter (ASCT2; also known as SLC1a5) and by repressing microRNA 23a/b (miR-23a/b), which normally blocks GLS translation (13, 14).”
• Tumor microenvironment derived exosomes pleiotropically modulate cancer cell metabolism (2016, background): “While many studies in cancer cell metabolism have highlighted higher compensatory glycolysis because of mitochondrial dysfunction; recent studies show that some tumors predominantly use glutamine under hypoxia or conditions mimicking hypoxia such as electron transport chain inhibition through reduct”
• MYC, Metabolism, and Cancer. (2015, background): “MYC, in essence, regulates virtually all genes involved in glycolysis and many in glutaminolysis (113, 114, 117, 118).”