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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Liu, Wei Dang, Chi V. Le, Anne Lane, Andrew N. Fan, Teresa W-m Hancock, Chad Phang, James M. |
| Description | Author Affiliation: Liu W ( Metabolism and Cancer Susceptibility Section, Basic Research Laboratory, National Cancer Institute, Frederick, MD 21702, USA. liuwei7997@gmail.com); |
| Abstract | In addition to glycolysis, the oncogenic transcription factor c-MYC (MYC) stimulates glutamine catabolism to fuel growth and proliferation of cancer cells through up-regulating glutaminase (GLS). Glutamine is converted to glutamate by GLS, entering the tricarboxylic acid cycle as an important energy source. Less well-recognized, glutamate can also be converted to proline through $Δ^{1}-pyrroline-5-carboxylate$ (P5C) and vice versa. This study suggests that some MYC-induced cellular effects are due to MYC regulation of proline metabolism. Proline oxidase, also known as proline dehydrogenase (POX/PRODH), the first enzyme in proline catabolism, is a mitochondrial tumor suppressor that inhibits proliferation and induces apoptosis. MiR-23b* mediates POX/PRODH down-regulation in human kidney tumors. MiR-23b* is processed from the same transcript as miR-23b; the latter inhibits the translation of GLS. Using MYC-inducible human Burkitt lymphoma model P493 and PC3 human prostate cancer cells, we showed that MYC suppressed POX/PRODH expression primarily through up-regulating miR-23b*. The growth inhibition in the absence of MYC was partially reversed by POX/PRODH knockdown, indicating the importance of suppression of POX/PRODH in MYC-mediated cellular effects. Interestingly, MYC not only inhibited POX/PRODH, but also markedly increased the enzymes of proline biosynthesis from glutamine, including P5C synthase and P5C reductase 1. MYC-induced proline biosynthesis from glutamine was directly confirmed using $^{13}C,^{15}N-glutamine$ as a tracer. The metabolic link between glutamine and proline afforded by MYC emphasizes the complexity of tumor metabolism. Further studies of the relationship between glutamine and proline metabolism should provide a deeper understanding of tumor metabolism while enabling the development of novel therapeutic strategies. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 23 |
| Volume Number | 109 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2012-06-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | DNA-Binding Proteins Metabolism Gene Expression Regulation, Enzymologic Physiology Glutamine MicroRNAs Proline Oxidase Proline Transcription Factors Blotting, Western Carbon Isotopes Cell Line, Tumor Chromatin Immunoprecipitation Gas Chromatography-Mass Spectrometry Genetics Gene Knockdown Techniques Nitrogen Isotopes Nuclear Magnetic Resonance, Biomolecular Oxidation-Reduction Pyrroline Carboxylate Reductases Reactive Oxygen Species Real-Time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Research Support, N.I.H., Extramural Research Support, N.I.H., Intramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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