Oncogene-Directed Alterations in Cancer Cell Metabolism

Trends in Cancer

Volumn 2, Issue 7, 2016, Pages 365-377

  Nagarajan, Arvindhan ^a   Malvi, Parmanand ^a   Wajapeyee, Narendra ^a,b  

^a YALE UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b YALE CANCER CENTER   (United States)

Author keywords

metabolic pathways; oncogene; precision cancer therapies.; tumor growth

Indexed keywords

B RAF KINASE; HEPARANASE; HEPARIN; HYDROXYMETHYLGLUTARYL COENZYME A REDUCTASE INHIBITOR; HYDROXYMETHYLGLUTARYL COENZYME A REDUCTASE KINASE; ISOCITRATE DEHYDROGENASE 1; ISOCITRATE DEHYDROGENASE 2; METFORMIN; RAPAMYCIN; SULFATASE; ANTINEOPLASTIC AGENT;

AMINO ACID METABOLISM; CANCER CELL; CARBOHYDRATE METABOLISM; CELL METABOLISM; DRUG TARGETING; HUMAN; LIPID METABOLISM; METABOLIC DISORDER; NEOPLASM; NONHUMAN; ONCOGENE; ONCOGENE MYC; ONCOGENE RAS; PERSONALIZED MEDICINE; PHASE 1 CLINICAL TRIAL (TOPIC); PHASE 2 CLINICAL TRIAL (TOPIC); PHASE 3 CLINICAL TRIAL (TOPIC); PRIORITY JOURNAL; REVIEW; ANIMAL; GENETICS; METABOLISM; MOLECULARLY TARGETED THERAPY;

ANIMALS; ANTINEOPLASTIC AGENTS; HUMANS; METABOLIC NETWORKS AND PATHWAYS; MOLECULAR TARGETED THERAPY; NEOPLASMS; ONCOGENES;

EID: 84977641041     PISSN: 24058033     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.trecan.2016.06.002     Document Type: Review

References (91)

1. 1 Hanahan, D., Weinberg, R.A., Hallmarks of cancer: the next generation. Cell 144 (2011), 646–674.
2. 2 Hanahan, D., Weinberg, R.A., The hallmarks of cancer. Cell 100 (2000), 57–70.
3. 3 Dang, C.V., MYC on the path to cancer. Cell 149 (2012), 22–35.
4. 4 Brodeur, G.M., et al. Amplification of N-myc in untreated human neuroblastomas correlates with advanced disease stage. Science 224 (1984), 1121–1124.
5. 5 Kohl, N.E., et al. Activated expression of the N-myc gene in human neuroblastomas and related tumors. Science 226 (1984), 1335–1337.
6. 6 Park, S., et al. Determination of binding constant of transcription factor myc-max/max-max and E-box DNA: the effect of inhibitors on the binding. Biochim. Biophys. Acta 1670 (2004), 217–228.
7. 7 Nakagawara, A., Ikeda, K., N-myc oncogene amplification and catecholamine metabolism in children with neuroblastoma. Lancet, 1, 1987, 559.
8. 8 Nakagawara, A., et al. Inverse correlation between N-myc amplification and catecholamine metabolism in children with advanced neuroblastoma. Surgery 107 (1990), 43–49.
9. 9 Tonini, G.P., et al. N-myc oncogene amplification and catecholamine metabolism in patients with neuroblastoma. Lancet, 2, 1987, 795.
10. 10 Pusch, O., et al. Cellular targets for activation by c-Myc include the DNA metabolism enzyme thymidine kinase. DNA Cell Biol. 16 (1997), 737–747.
11. 11 Shim, H., et al. c-Myc transactivation of LDH-A: implications for tumor metabolism and growth. Proc. Natl. Acad. Sci. U.S.A. 94 (1997), 6658–6663.
12. 12 Maya-Mendoza, A., et al. Myc and Ras oncogenes engage different energy metabolism programs and evoke distinct patterns of oxidative and DNA replication stress. Mol. Oncol. 9 (2015), 601–616.
13. 13 Edmunds, L.R., et al. c-Myc programs fatty acid metabolism and dictates acetyl-CoA abundance and fate. J. Biol. Chem. 289 (2014), 25382–25392.
14. 14 de la Cova, C., et al. Supercompetitor status of Drosophila Myc cells requires p53 as a fitness sensor to reprogram metabolism and promote viability. Cell Metab. 19 (2014), 470–483.
15. 15 Liu, W., et al. Reprogramming of proline and glutamine metabolism contributes to the proliferative and metabolic responses regulated by oncogenic transcription factor c-MYC. Proc. Natl. Acad. Sci. U.S.A. 109 (2012), 8983–8988.
16. 16 Gao, P., et al. c-Myc suppression of miR-23a/b enhances mitochondrial glutaminase expression and glutamine metabolism. Nature 458 (2009), 762–765.
17. 17 Mannava, S., et al. Direct role of nucleotide metabolism in C-MYC-dependent proliferation of melanoma cells. Cell Cycle 7 (2008), 2392–2400.
18. 18 Shroff, E.H., et al. MYC oncogene overexpression drives renal cell carcinoma in a mouse model through glutamine metabolism. Proc. Natl. Acad. Sci. U.S.A. 112 (2015), 6539–6544.
19. 19 Curtin, J.A., et al. Distinct sets of genetic alterations in melanoma. N. Engl. J. Med. 353 (2005), 2135–2147.
20. 20 Neri, A., et al. Analysis of RAS oncogene mutations in human lymphoid malignancies. Proc. Natl. Acad. Sci. U.S.A. 85 (1988), 9268–9272.
21. 21 Bacher, U., et al. Implications of NRAS mutations in AML: a study of 2502 patients. Blood 107 (2006), 3847–3853.
22. 22 Guo, G., et al. Whole-genome and whole-exome sequencing of bladder cancer identifies frequent alterations in genes involved in sister chromatid cohesion and segregation. Nat. Genet. 45 (2013), 1459–1463.
23. 23 Agrawal, N., et al. Exome sequencing of head and neck squamous cell carcinoma reveals inactivating mutations in NOTCH1. Science 333 (2011), 1154–1157.
24. 24 Davies, H., et al. Mutations of the BRAF gene in human cancer. Nature 417 (2002), 949–954.
25. 25 Downward, J., Targeting RAS signalling pathways in cancer therapy. Nat. Rev. Cancer 3 (2003), 11–22.
26. 26 Pakala, R., et al. Polyamine metabolism and interconversion in NIH 3T3 and ras-transfected NIH 3T3 cells. Cancer Res. 48 (1988), 3336–3340.
27. 27 Chiarugi, V.P., et al. Signal transduction in EJ-H-ras-transformed cells: de novo synthesis of diacylglycerol and subversion of agonist-stimulated inositol lipid metabolism. FEBS Lett. 252 (1989), 129–134.
28. 28 Huang, M., et al. Enhancement of inositol phospholipid metabolism and activation of protein kinase C in ras-transformed rat fibroblasts. J. Biol. Chem. 263 (1988), 17975–17980.
29. 29 Milligan, G., et al. Identification of the pertussis and cholera toxin substrates in normal and N-ras transformed NIH3T3 fibroblasts and an assessment of their involvement in bombesin-stimulation of inositol phospholipid metabolism. Oncogene 4 (1989), 659–663.
30. 30 Chiaradonna, F., et al. Ras-dependent carbon metabolism and transformation in mouse fibroblasts. Oncogene 25 (2006), 5391–5404.
31. 31 Ying, H., et al. Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism. Cell 149 (2012), 656–670.
32. 32 Son, J., et al. Glutamine supports pancreatic cancer growth through a KRAS-regulated metabolic pathway. Nature 496 (2013), 101–105.
33. 33 Commisso, C., et al. Macropinocytosis of protein is an amino acid supply route in Ras-transformed cells. Nature 497 (2013), 633–637.
34. 34 Lim, J.P., Gleeson, P.A., Macropinocytosis: an endocytic pathway for internalising large gulps. Immunol. Cell. Biol. 89 (2011), 836–843.
35. 35 Haq, R., et al. Oncogenic BRAF regulates oxidative metabolism via PGC1alpha and MITF. Cancer Cell 23 (2013), 302–315.
36. 36 Scott, D.A., et al. Comparative metabolic flux profiling of melanoma cell lines: beyond the Warburg effect. J. Biol. Chem. 286 (2011), 42626–42634.
37. 37 Trousil, S., Zheng, B., Addicted to AA (Acetoacetate): A Point of Convergence between Metabolism and BRAF Signaling. Mol. Cell 59 (2015), 333–334.
38. 38 Kang, H.B., et al. Metabolic Rewiring by Oncogenic BRAF V600E Links Ketogenesis Pathway to BRAF-MEK1 Signaling. Mol. Cell 59 (2015), 345–358.
39. 39 Kaplon, J., et al. A key role for mitochondrial gatekeeper pyruvate dehydrogenase in oncogene-induced senescence. Nature 498 (2013), 109–112.
40. 40 Parsons, D.W., et al. An integrated genomic analysis of human glioblastoma multiforme. Science 321 (2008), 1807–1812.
41. 41 Mardis, E.R., et al. Recurring mutations found by sequencing an acute myeloid leukemia genome. N. Engl. J. Med. 361 (2009), 1058–1066.
42. 42 Yan, H., et al. IDH1 and IDH2 mutations in gliomas. N. Engl. J. Med. 360 (2009), 765–773.
43. 43 Locasale, J.W., Cantley, L.C., Metabolic flux and the regulation of mammalian cell growth. Cell Metab. 14 (2011), 443–451.
44. 44 Warburg, O., On the origin of cancer cells. Science 123 (1956), 309–314.
45. 45 Hsu, P.P., Sabatini, D.M., Cancer cell metabolism: Warburg and beyond. Cell 134 (2008), 703–707.
46. 46 Kennedy, K.M., Dewhirst, M.W., Tumor metabolism of lactate: the influence and therapeutic potential for MCT and CD147 regulation. Future Oncol. 6 (2010), 127–148.
47. 47 van Horssen, R., et al. Cancer cell metabolism regulates extracellular matrix degradation by invadopodia. Eur. J. Cell Biol. 92 (2013), 113–121.
48. 48 Cardone, R.A., et al. The role of disturbed pH dynamics and the Na+/H+ exchanger in metastasis. Nat. Rev. Cancer 5 (2005), 786–795.
49. 49 Lu, H., et al. Hypoxia-inducible factor 1 activation by aerobic glycolysis implicates the Warburg effect in carcinogenesis. J. Biol. Chem. 277 (2002), 23111–23115.
50. 50 Colegio, O.R., et al. Functional polarization of tumour-associated macrophages by tumour-derived lactic acid. Nature 513 (2014), 559–563.
51. 51 Vega-Naredo, I., et al. Mitochondrial metabolism directs stemness and differentiation in P19 embryonal carcinoma stem cells. Cell Death Differ. 21 (2014), 1560–1574.
52. 52 Hamanaka, R.B., Chandel, N.S., Targeting glucose metabolism for cancer therapy. J. Exp. Med. 209 (2012), 211–215.
53. 53 Wang, G.L., et al. Hypoxia-inducible factor 1 is a basic-helix-loop-helix-PAS heterodimer regulated by cellular O2 tension. Proc. Natl. Acad. Sci. U.S.A. 92 (1995), 5510–5514.
54. 54 Kaelin, W.G. Jr., Ratcliffe, P.J., Oxygen sensing by metazoans: the central role of the HIF hydroxylase pathway. Mol. Cell 30 (2008), 393–402.
55. 55 Su, T.S., et al. Elevation of facilitated glucose-transporter messenger RNA in human hepatocellular carcinoma. Hepatology 11 (1990), 118–122.
56. 56 Yamamoto, T., et al. Over-expression of facilitative glucose transporter genes in human cancer. Biochem. Biophys. Res. Commun. 170 (1990), 223–230.
57. 57 Nishioka, T., et al. Distribution of the glucose transporters in human brain tumors. Cancer Res. 52 (1992), 3972–3979.
58. 58 Xu, W., et al. Oncometabolite 2-hydroxyglutarate is a competitive inhibitor of alpha-ketoglutarate-dependent dioxygenases. Cancer Cell 19 (2011), 17–30.
59. 59 Cardaci, S., Ciriolo, M.R., TCA Cycle Defects and Cancer: When Metabolism Tunes Redox State. Int. J. Cell Biol., 2012, 2012, 161837.
60. 60 Duvel, K., et al. Activation of a metabolic gene regulatory network downstream of mTOR complex 1. Mol. Cell 39 (2010), 171–183.
61. 61 Stanton, R.C., et al. Rapid release of bound glucose-6-phosphate dehydrogenase by growth factors. Correlation with increased enzymatic activity. J. Biol. Chem. 266 (1991), 12442–12448.
62. 62 Lin, R., et al. 6-Phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumour growth by inhibiting LKB1-AMPK signalling. Nat. Cell Biol. 17 (2015), 1484–1496.
63. 63 Horton, J.D., et al. Combined analysis of oligonucleotide microarray data from transgenic and knockout mice identifies direct SREBP target genes. Proc. Natl. Acad. Sci. U.S.A. 100 (2003), 12027–12032.
64. 64 Hatzivassiliou, G., et al. ATP citrate lyase inhibition can suppress tumor cell growth. Cancer Cell 8 (2005), 311–321.
65. 65 Chajes, V., et al. Acetyl-CoA carboxylase alpha is essential to breast cancer cell survival. Cancer Res. 66 (2006), 5287–5294.
66. 66 Vander Haar, E., et al. Insulin signalling to mTOR mediated by the Akt/PKB substrate PRAS40. Nat. Cell Biol. 9 (2007), 316–323.
67. 67 Shaw, R.J., et al. The LKB1 tumor suppressor negatively regulates mTOR signaling. Cancer Cell 6 (2004), 91–99.
68. 68 Wullschleger, S., et al. TOR signaling in growth and metabolism. Cell 124 (2006), 471–484.
69. 69 Bar-Peled, L., Sabatini, D.M., Regulation of mTORC1 by amino acids. Trends Cell Biol. 24 (2014), 400–406.
70. 70 Amelio, I., et al. Serine and glycine metabolism in cancer. Trends Biochem. Sci. 39 (2014), 191–198.
71. 71 Uyttenhove, C., et al. Evidence for a tumoral immune resistance mechanism based on tryptophan degradation by indoleamine 2,3-dioxygenase. Nat. Med. 9 (2003), 1269–1274.
72. 72 Dillon, B.J., et al. Incidence and distribution of argininosuccinate synthetase deficiency in human cancers: a method for identifying cancers sensitive to arginine deprivation. Cancer 100 (2004), 826–833.
73. 73 Komada, Y., et al. Apoptotic cell death of human T lymphoblastoid cells induced by arginine deiminase. Int. J. Hematol. 65 (1997), 129–141.
74. 74 Zhang, B., et al. Asparagine synthetase is an independent predictor of surgical survival and a potential therapeutic target in hepatocellular carcinoma. Br. J. Cancer 109 (2013), 14–23.
75. 75 Knelson, E.H., et al. Heparan sulfate signaling in cancer. Trends Biochem. Sci. 39 (2014), 277–288.
76. 76 Haimovitz-Friedman, A., et al. Ceramide signaling in apoptosis. Br. Med. Bull. 53 (1997), 539–553.
77. 77 Ponzoni, M., et al. Differential effects of N-(4-hydroxyphenyl)retinamide and retinoic acid on neuroblastoma cells: apoptosis versus differentiation. Cancer Res. 55 (1995), 853–861.
78. 78 Dhillon, A.S., et al. MAP kinase signalling pathways in cancer. Oncogene 26 (2007), 3279–3290.
79. 79 Li, W., et al. Targeting AMPK for cancer prevention and treatment. Oncotarget 6 (2015), 7365–7378.
80. 80 Chiacchiera, F., Simone, C., The AMPK-FoxO3A axis as a target for cancer treatment. Cell Cycle 9 (2010), 1091–1096.
81. 81 Morales, D.R., Morris, A.D., Metformin in cancer treatment and prevention. Annu. Rev. Med. 66 (2015), 17–29.
82. 82 Zhang, Z.J., et al. Metformin for liver cancer prevention in patients with type 2 diabetes: a systematic review and meta-analysis. J. Clin. Endocrinol. Metab. 97 (2012), 2347–2353.
83. 83 Yang, Y., Metformin for cancer prevention. Front Med. 5 (2011), 115–117.
84. 84 Faller, W.J., et al. mTORC1-mediated translational elongation limits intestinal tumour initiation and growth. Nature 517 (2015), 497–500.
85. 85 Cloughesy, T.F., et al. Antitumor activity of rapamycin in a Phase I trial for patients with recurrent PTEN-deficient glioblastoma. PLoS Med., 5, 2008, e8.
86. 86 Wick, A.N., et al. Localization of the primary metabolic block produced by 2-deoxyglucose. J. Biol. Chem. 224 (1957), 963–969.
87. 87 Pelicano, H., et al. Glycolysis inhibition for anticancer treatment. Oncogene 25 (2006), 4633–4646.
88. 88 Vlodavsky, I., et al. Inhibition of tumor metastasis by heparanase inhibiting species of heparin. Invasion Metastasis 14 (1994), 290–302.
89. 89 Ott, P.A., et al. Phase I/II study of pegylated arginine deiminase (ADI-PEG 20) in patients with advanced melanoma. Invest. New Drugs 31 (2013), 425–434.
90. 90 Yau, T., et al. A phase 1 dose-escalating study of pegylated recombinant human arginase 1 (Peg-rhArg1) in patients with advanced hepatocellular carcinoma. Invest. New Drugs 31 (2013), 99–107.
91. 91 Agrawal, N.R., et al. A Phase I-II trial of polyethylene glycol-conjugated L-asparaginase in patients with multiple myeloma. Cancer 98 (2003), 94–99.