Abstract：
:Because MYC plays a causal role in many human cancers, including those with hypoxic and nutrient-poor tumor microenvironments, we have determined the metabolic responses of a MYC-inducible human Burkitt lymphoma model P493 cell line to aerobic and hypoxic conditions, and to glucose deprivation, using stable isotope-resolved metabolomics. Using [U-(13)C]-glucose as the tracer, both glucose consumption and lactate production were increased by MYC expression and hypoxia. Using [U-(13)C,(15)N]-glutamine as the tracer, glutamine import and metabolism through the TCA cycle persisted under hypoxia, and glutamine contributed significantly to citrate carbons. Under glucose deprivation, glutamine-derived fumarate, malate, and citrate were significantly increased. Their (13)C-labeling patterns demonstrate an alternative energy-generating glutaminolysis pathway involving a glucose-independent TCA cycle. The essential role of glutamine metabolism in cell survival and proliferation under hypoxia and glucose deficiency makes them susceptible to the glutaminase inhibitor BPTES and hence could be targeted for cancer therapy.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Le A,Lane AN,Hamaker M,Bose S,Gouw A,Barbi J,Tsukamoto T,Rojas CJ,Slusher BS,Zhang H,Zimmerman LJ,Liebler DC,Slebos RJ,Lorkiewicz PK,Higashi RM,Fan TW,Dang CVdoi
10.1016/j.cmet.2011.12.009subject
Has Abstractpub_date
2012-01-04 00:00:00pages
110-21issue
1eissn
1550-4131issn
1932-7420pii
S1550-4131(11)00468-2journal_volume
15pub_type
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