Metabolic assessment of a novel chronic myelogenous leukemic cell line and an imatinib resistant subline by 1H NMR spectroscopy

Metabolomics

Volumn 6, Issue 3, 2010, Pages 439-450

  Dewar, Brian J ^a,c   Keshari, Kayvan ^c   Jeffries, Rex ^c   Dzeja, Petras ^d   Graves, Lee M ^a,b   Macdonald, Jeffrey M ^a,c  

^a UNIVERSITY OF NORTH CAROLINA   (United States)

^b UNIVERSITY OF NORTH CAROLINA SCHOOL OF MEDICINE   (United States)

^c NORTH CAROLINA STATE UNIVERSITY   (United States)

^d MAYO CLINIC   (United States)

Author keywords

1H NMR spectroscopy; Chronic myelogenous leukemia; Creatine; Drug resistance; Imatinib; Metabolomics

Indexed keywords

EID: 77954458737     PISSN: 15733882     EISSN: 15733890     Source Type: Journal    
DOI: 10.1007/s11306-010-0204-0     Document Type: Article

References (41)

1. Ackerstaff, E., Glunde, K., & Bhujwalla, Z. M. (2003). Choline phospholipid metabolism: A target in cancer cells? Journal of Cellular Biochemistry, 90, 525-533.
2. Apperley, J. F. (2007). Part I: Mechanisms of resistance to imatinib in chronic myeloid leukaemia. Lancet Oncology, 8, 1018-1029.
3. Barnes, K., McIntosh, E., Whetton, A. D., Daley, G. Q., Bentley, J., & Baldwin, S. A. (2005). Chronic myeloid leukaemia: An investigation into the role of Bcr-Abl-induced abnormalities in glucose transport regulation. Oncogene, 24, 3257-3267.
4. Boren, J., Cascante, M., Marin, S., Comin-Anduix, B., Centelles, J. J., Lim, S., et al. (2001). Gleevec (STI571) influences metabolic enzyme activities and glucose carbon flow toward nucleic acid and fatty acid synthesis in myeloid tumor cells. Journal of Biological Chemistry, 276, 37747-37753.
5. Boros, L. G., Brackett, D. J., & Harrigan, G. G. (2003). Metabolic biomarker and kinase drug target discovery in cancer using stable isotope-based dynamic metabolic profiling (SIDMAP). Current Cancer Drug Targets, 3, 445-453.
6. Campbell, L. J., Patsouris, C., Rayeroux, K. C., Somana, K., Januszewicz, E. H., & Szer, J. (2002). BCR/ABL amplification in chronic myelocytic leukemia blast crisis following imatinib mesylate administration. Cancer Genetics and Cytogenetics, 139, 30-33.
7. Daley, G. Q., van Etten, R. A., & Baltimore, D. (1990). Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome. Science, 247, 824-830.
8. DeBerardinis, R. J., Mancuso, A., Daikhin, E., Nissim, I., Yudkoff, M., Wehrli, S., et al. (2007). Beyond aerobic glycolysis: Transformed cells can engage in glutamine metabolism that exceeds the requirement for protein and nucleotide synthesis. Proceedings of the National Academy of Sciences of the United States of America, 104, 19345-19350.
9. Deininger, M. W., Goldman, J. M., Lydon, N., & Melo, J. V. (1997). The tyrosine kinase inhibitor CGP57148B selectively inhibits the growth of BCR-ABL-positive cells. Blood, 90, 3691-3698.
10. Dolder, M., Walzel, B., Speer, O., Schlattner, U., & Wallimann, T. (2003). Inhibition of the mitochondrial permeability transition by creatine kinase substrates. Requirement for microcompartmentation. Journal of Biological Chemistry, 278, 17760-17766.
11. Donato, N. J., Wu, J. Y., Stapley, J., Gallick, G., Lin, H., Arlinghaus, R., et al. (2003). BCR-ABL independence and LYN kinase overexpression in chronic myelogenous leukemia cells selected for resistance to STI571. Blood, 101, 690-698.
12. Druker, B. J., Tamura, S., Buchdunger, E., Ohno, S., Segal, G. M., Fanning, S., et al. (1996). Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells. Nature Medicine, 2, 561-566.
13. Franks, S. E., Smith, M. R., Arias-Mendoza, F., Shaller, C., Padavic-Shaller, K., Kappler, F., et al. (2002). Phosphomonoester concentrations differ between chronic lymphocytic leukemia cells and normal human lymphocytes. Leukemia Research, 26, 919-926.
14. Glunde, K., Ackerstaff, E., Mori, N., Jacobs, M. A., & Bhujwalla, Z. M. (2006). Choline phospholipid metabolism in cancer: Consequences for molecular pharmaceutical interventions. Molecular Pharmaceutics, 3, 496-506.
15. Gorre, M. E., Mohammed, M., Ellwood, K., Hsu, N., Paquette, R., Rao, P. N., et al. (2001). Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Science, 293, 876-880.
16. Gottschalk, S., Anderson, N., Hainz, C., Eckhardt, S. G., & Serkova, N. J. (2004). Imatinib (STI571)-mediated changes in glucose metabolism in human leukemia BCR-ABL-positive cells. Clinical Cancer Research, 10, 6661-6668.
17. Griffin, J. L. (2003). Metabonomics: NMR spectroscopy and pattern recognition analysis of body fluids and tissues for characterisation of xenobiotic toxicity and disease diagnosis. Current Opinion in Chemical Biology, 7, 648-654.
18. Huxtable, R. J. (1992). Physiological actions of taurine. Physiological Reviews, 72, 101-163.
19. Illmer, T., Schaich, M., Platzbecker, U., Freiberg-Richter, J., Oelschlagel, U., von Bonin, M., et al. (2004). P-glycoprotein-mediated drug efflux is a resistance mechanism of chronic myelogenous leukemia cells to treatment with imatinib mesylate. Leukemia, 18, 401-408.
20. Ito, T., Tanaka, H., & Kimura, A. (2007). Establishment and characterization of a novel imatinib-sensitive chronic myeloid leukemia cell line MYL, and an imatinib-resistant subline MYL-R showing overexpression of Lyn. European Journal of Haematology, 78, 417-431.
21. Jiang, X. R., Yang, M., Morris, C. J., Newland, A. C., Naughton, D. P., Blake, D. R., et al. (1993). High field proton NMR investigations of the metabolic profiles of multidrug-sensitive and -resistant leukaemic cell lines: Evidence for diminished taurine levels in multidrug-resistant cells. Free Radical Research Communications, 19, 355-369.
22. Kaadige, M. R., Looper, R. E., Kamalanaadhan, S., & Ayer, D. E. (2009). Glutamine-dependent anapleurosis dictates glucose uptake and cell growth by regulating MondoA transcriptional activity. Proceedings of the National Academy of Sciences of the United States of America, 106, 14878-14883.
23. Kaplan, O., van Zijl, P. C., & Cohen, J. S. (1990). Information from combined 1H and 31P NMR studies of cell extracts: Differences in metabolism between drug-sensitive and drug-resistant MCF-7 human breast cancer cells. Biochemical and Biophysical Research Communications, 169, 383-390.
24. Keshari, K. R., Kurhanewicz, J., Jeffries, R. E., Wilson, D. M., Dewar, B. J., van Criekinge, M., et al. (2010). Hyperpolarized (13)C spectroscopy and an NMR-compatible bioreactor system for the investigation of real-time cellular metabolism. Magnetic Resonance in Medicine, 63, 322-329.
25. Klawitter, J., Anderson, N., Christians, U., Leibfritz, D., Eckhardt, S. G., & Serkova, N. J. (2009a). Time-dependent effects of imatinib in human leukaemia cells: A kinetic NMR-profiling study. British Journal of Cancer, 100, 923-931.
26. Klawitter, J., Kominsky, D. J., Brown, J. L., Christians, U., Leibfritz, D., Melo, J. V., et al. (2009b). Metabolic characteristics of imatinib resistance in chronic myeloid leukaemia cells. British Journal of Pharmacology, 158, 588-600.
27. Kominsky, D. J., Klawitter, J., Brown, J. L., Boros, L. G., Melo, J. V., Eckhardt, S. G., et al. (2009). Abnormalities in glucose uptake and metabolism in imatinib-resistant human BCR-ABL-positive cells. Clinical Cancer Research, 15, 3442-3450.
28. Kuwazuru, Y., Yoshimura, A., Hanada, S., Ichikawa, M., Saito, T., Uozumi, K., et al. (1990). Expression of the multidrug transporter, P-glycoprotein, in chronic myelogenous leukaemia cells in blast crisis. British Journal of Haematology, 74, 24-29.
29. Loike, J. D., Kozler, V. F., & Silverstein, S. C. (1984). Creatine kinase expression and creatine phosphate accumulation are developmentally regulated during differentiation of mouse and human monocytes. Journal of Experimental Medicine, 159, 746-757.
30. Loike, J. D., Somes, M., & Silverstein, S. C. (1986). Creatine uptake, metabolism, and efflux in human monocytes and macrophages. American Journal of Physiology, 251, C128-C135.
31. Maharjan, R. P., & Ferenci, T. (2003). Global metabolite analysis: The influence of extraction methodology on metabolome profiles of Escherichia coli. Analytical Biochemistry, 313, 145-154.
32. Mahon, F. X., Deininger, M. W., Schultheis, B., Chabrol, J., Reiffers, J., Goldman, J. M., et al. (2000). Selection and characterization of BCR-ABL positive cell lines with differential sensitivity to the tyrosine kinase inhibitor STI571: Diverse mechanisms of resistance. Blood, 96, 1070-1079.
33. Melo, J. V., Gordon, D. E., Cross, N. C., & Goldman, J. M. (1993). The ABL-BCR fusion gene is expressed in chronic myeloid leukemia. Blood, 81, 158-165.
34. O'Gorman, E., Beutner, G., Dolder, M., Koretsky, A. P., Brdiczka, D., & Wallimann, T. (1997). The role of creatine kinase in inhibition of mitochondrial permeability transition. FEBS Letters, 414, 253-257.
35. Opstad, K. S., Bell, B. A., Griffiths, J. R., & Howe, F. A. (2009). Taurine: A potential marker of apoptosis in gliomas. British Journal of Cancer, 100, 789-794.
36. Reo, N. V. (2002). NMR-based metabolomics. Drug and Chemical Toxicology, 25, 375-382.
37. Rowley, J. D. (1973). Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining. Nature, 243, 290-293.
38. Serkova, N., & Boros, L. G. (2005). Detection of resistance to imatinib by metabolic profiling: Clinical and drug development implications. American Journal of Pharmacogenomics, 5, 293-302.
39. Weljie, A. M., Newton, J., Mercier, P., Carlson, E., & Slupsky, C. M. (2006). Targeted profiling: Quantitative analysis of 1H NMR metabolomics data. Analytical Chemistry, 78, 4430-4442.
40. Wu, Q. D., Wang, J. H., Fennessy, F., Redmond, H. P., & Bouchier-Hayes, D. (1999). Taurine prevents high-glucose-induced human vascular endothelial cell apoptosis. American Journal of Physiology, 277, C1229-C1238.
41. Wyss, M., & Kaddurah-Daouk, R. (2000). Creatine and creatinine metabolism. Physiological Reviews, 80, 1107-1213.