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Journal of Biomedicine and Biotechnology
Volume 2012 (2012), Article ID 654291, 8 pages
Analyzing Gene Expression Profile in K562 Cells Exposed to Sodium Valproate Using Microarray Combined with the Connectivity Map Database
1Department of Hematology, The Third Affiliated Hospital of Sun Yat-sen University, Guangdong 510630, Guangzhou, China
2Prenatal Diagnosis Center, The Women and Children Hospital of Guangdong Province, Guangdong 510010, Guangzhou, China
3Key Laboratory of Department of Health of Guangdong Province for Maternal and Children Metabolic-Genetic Disease Diagnosis, Guangdong 510010, Guangzhou, China
4Department of Hematology, First Affiliated Hospital of Sun Yat-sen University, Guangdong 510080, Guangzhou, China
5Department of Hematology, Anhui Provincial Hospital Affiliated to Anhui Medical University, Anhui 230001, Hefei, China
6Department of Hematology, Guizhou Provincial Hospital, Guizhou 550002, Guiyang, China
Received 6 February 2012; Revised 26 March 2012; Accepted 9 April 2012
Academic Editor: Eric W. Lam
Copyright © 2012 Xiang-Zhong Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
- A. H. Wang, L. Wei, L. Chen et al., “Synergistic effect of bortezomib and valproic acid treatment on the proliferation and apoptosis of acute myeloid leukemia and myelodysplastic syndrome cells,” Annals of Hematology, vol. 90, no. 8, pp. 917–931, 2011.
- B. Kircher, P. Schumacher, A. Petzer et al., “Anti-leukemic activity of valproic acid and imatinib mesylate on human Ph+ ALL and CML cells in vitro,” European Journal of Haematology, vol. 83, no. 1, pp. 48–56, 2009.
- F. Buchi, R. Pastorelli, G. Ferrari et al., “Acetylome and phosphoproteome modifications in imatinib resistant chronic myeloid leukaemia cells treated with valproic acid,” Leukemia Research, vol. 35, no. 7, pp. 921–931, 2011.
- G. Iacomino, M. C. Medici, and G. L. Russo, “Valproic acid sensitizes K562 erythroleukemia cells to TRAIL/Apo2L-induced apoptosis,” Anticancer Research A, vol. 28, no. 2, pp. 855–864, 2008.
- E. S. Sung, A. Kim, J. S. Park, J. Chung, M. H. Kwon, and Y. S. Kim, “Histone deacetylase inhibitors synergistically potentiate death receptor 4-mediated apoptotic cell death of human T-cell acute lymphoblastic leukemia cells,” Apoptosis, vol. 15, no. 10, pp. 1256–1269, 2010.
- L. Lagneaux, N. Gillet, B. Stamatopoulos et al., “Valproic acid induces apoptosis in chronic lymphocytic leukemia cells through activation of the death receptor pathway and potentiates TRAIL response,” Experimental Hematology, vol. 35, no. 10, pp. 1527–1537, 2007.
- J. Stieglmaier, E. Bremer, C. Kellner et al., “Selective induction of apoptosis in leukemic B-lymphoid cells by a CD19-specific TRAIL fusion protein,” Cancer Immunology, Immunotherapy, vol. 57, no. 2, pp. 233–246, 2008.
- E. Raffoux, A. Cras, C. Recher, et al., “Phase 2 clinical trial of 5-azacitidine, valproic acid, and all-trans retinoic acid in patients with high-risk acute myeloid leukemia or myelodysplastic syndrome,” Oncotarget, vol. 1, pp. 34–42, 2010.
- G. Bug, M. Ritter, B. Wassmann et al., “Clinical trial of valproic acid and all-trans retinoic acid in patients with poor-risk acute myeloid leukemia,” Cancer, vol. 104, no. 12, pp. 2717–2725, 2005.
- A. Kuendgen, M. Schmid, R. Schlenk et al., “The histone deacetylase (HDAC) inhibitor valproic acid as monotherapy or in combination with all-trans retinoic acid in patients with acute myeloid leukemia,” Cancer, vol. 106, no. 1, pp. 112–119, 2006.
- C. Pilatrino, D. Cilloni, E. Messa et al., “Increase in platelet count in older, poor-risk patients with acute myeloid leukemia or myelodysplastic syndrome treated with valproic acid and all-trans retinoic acid,” Cancer, vol. 104, no. 1, pp. 101–109, 2005.
- B. Stamatopoulos, N. Meuleman, C. De Bruyn et al., “Antileukemic activity of valproic acid in chronic lymphocytic leukemia B cells defined by microarray analysis,” Leukemia, vol. 23, no. 12, pp. 2281–2289, 2009.
- F. L. Khanim, C. A. Bradbury, J. Arrazi et al., “Elevated FOSB-expression; a potential marker of valproate sensitivity in AML,” British Journal of Haematology, vol. 144, no. 3, pp. 332–341, 2009.
- Y. C. Cheng, H. Lin, M. J. Huang, J. M. Chow, S. Lin, and H. E. Liu, “Downregulation of c-Myc is critical for valproic acid-induced growth arrest and myeloid differentiation of acute myeloid leukemia,” Leukemia Research, vol. 31, no. 10, pp. 1403–1411, 2007.
- W. Fayad, M. Fryknäs, S. Brnjic, M. H. Olofsson, R. Larsson, and S. Linder, “Identification of a novel topoisomerase inhibitor effective in cells overexpressing drug efflux transporters,” Plos ONE, vol. 4, no. 10, Article ID e7238, 2009.
- J. Gheeya, P. Johansson, Q. R. Chen et al., “Expression profiling identifies epoxy anthraquinone derivative as a DNA topoisomerase inhibitor,” Cancer Letters, vol. 293, no. 1, pp. 124–131, 2010.
- H. Hieronymus, J. Lamb, K. N. Ross et al., “Gene expression signature-based chemical genomic prediction identifies a novel class of HSP90 pathway modulators,” Cancer Cell, vol. 10, no. 4, pp. 321–330, 2006.
- Z. Wen, Z. Wang, S. Wang et al., “Discovery of molecular mechanisms of traditional Chinese medicinal formula Si-Wu-Tang using gene expression Microarray and Connectivity Map,” Plos ONE, vol. 6, no. 3, Article ID e18278, 2011.
- D. K. Slonim, K. Koide, K. L. Johnson et al., “Functional genomic analysis of amniotic fluid cell-free mRNA suggests that oxidative stress is significant in Down syndrome fetuses,” Proceedings of the National Academy of Sciences of the United States of America, vol. 106, no. 23, pp. 9425–9429, 2009.
- X. Z. Zhang, A. H. Yin, X. Y. Zhu, Q. Ding, C. H. Wang, and Y. X. Chen, “Using an exon microarray to identify a global profile of gene expression and alternative splicing in K562 cells exposed to sodium valproate,” Oncology Reports, vol. 27, pp. 1258–1265, 2012.
- T. A. Patterson, E. K. Lobenhofer, S. B. Fulmer-Smentek et al., “Performance comparison of one-color and two-color platforms within the MicroArray Quality Control (MAQC) project,” Nature Biotechnology, vol. 24, no. 9, pp. 1140–1150, 2006.
- K. J. Livak and T. D. Schmittgen, “Analysis of relative gene expression data using real-time quantitative PCR and the 2-ΔΔCT method,” Methods, vol. 25, no. 4, pp. 402–408, 2001.
- J. Lamb, E. D. Crawford, D. Peck et al., “The connectivity map: using gene-expression signatures to connect small molecules, genes, and disease,” Science, vol. 313, no. 5795, pp. 1929–1935, 2006.
- J. Lamb, “The Connectivity Map: a new tool for biomedical research,” Nature Reviews Cancer, vol. 7, no. 1, pp. 54–60, 2007.
- J. J. Kovacs, P. J. M. Murphy, S. Gaillard et al., “HDAC6 regulates Hsp90 acetylation and chaperone-dependent activation of glucocorticoid receptor,” Molecular Cell, vol. 18, no. 5, pp. 601–607, 2005.
- W. Gu and R. G. Roeder, “Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain,” Cell, vol. 90, no. 4, pp. 595–606, 1997.
- A. Romanski, B. Bacic, G. Bug et al., “Use of a novel histone deacetylase inhibitor to induce apoptosis in cell lines of acute lymphoblastic leukemia,” Haematologica, vol. 89, no. 4, pp. 419–426, 2004.
- A. Morotti, D. Cilioni, F. Messa et al., “Valproate enhances imatinib-induced growth arrest and apoptosis in chronic myeloid leukemia cells,” Cancer, vol. 106, no. 5, pp. 1188–1196, 2006.
- H. Fredly, C. Stapnes Bjørnsen, B. T. Gjertsen, and Ø. Bruserud, “Combination of the histone deacetylase inhibitor valproic acid with oral hydroxyurea or 6-mercaptopurin can be safe and effective in patients with advanced acute myeloid leukaemia—a report of five cases,” Hematology, vol. 15, no. 5, pp. 338–343, 2010.
- J. S. Carew, F. J. Giles, and S. T. Nawrocki, “Histone deacetylase inhibitors: mechanisms of cell death and promise in combination cancer therapy,” Cancer Letters, vol. 269, no. 1, pp. 7–17, 2008.
- R. R. Rosato, J. A. Almenara, Y. Dai, and S. Grant, “Simultaneous activation of the intrinsic and extrinsic pathways by histone deacetylase (HDAC) inhibitors and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) synergistically induces mitochondrial damage and apoptosis in human leukemia cells,” Molecular Cancer Therapeutics, vol. 2, no. 12, pp. 1273–1284, 2003.
- L. A. Petruccelli, D. Dupéré-Richer, F. Pettersson, H. Retrouvey, S. Skoulikas, and W. H. Miller Jr., “Vorinostat induces reactive oxygen species and dna damage in acute myeloid leukemia cells,” Plos ONE, vol. 6, no. 6, Article ID e20987, 2011.
- B. Brodska and A. Holoubek, “Generation of reactive oxygen species during apoptosis induced by DNA-damaging agents and/or histone deacetylase inhibitors,” Oxidative Medicine and Cellular Longevity, vol. 2011, Article ID 253529, 7 pages, 2011.
- J. M. Adams and S. Cory, “The Bcl-2 apoptotic switch in cancer development and therapy,” Oncogene, vol. 26, no. 9, pp. 1324–1337, 2007.
- V. Tong, X. W. Teng, T. K. H. Chang, and F. S. Abbott, “Valproic acid II: effects on oxidative stress, mitochondrial membrane potential, and cytotoxicity in glutathione-depleted rat hepatocytes,” Toxicological Sciences, vol. 86, no. 2, pp. 436–443, 2005.
- K. H. Schulpis, C. Lazaropoulou, S. Regoutas et al., “Valproic acid monotherapy induces DNA oxidative damage,” Toxicology, vol. 217, no. 2-3, pp. 228–232, 2006.
- E. W. Tung and L. M. Winn, “Valproic acid increases formation of reactive oxygen species and induces apoptosis in postimplantation embryos: a role for oxidative stress in valproic acid-induced neural tube defects,” Molecular Pharmacology, vol. 80, pp. 979–987, 2011.
- T. Skorski, P. Kanakaraj, M. Nieborowska-Skorska et al., “Phosphatidylinositol-3 kinase activity is regulated by BCR/ABL and is required for the growth of Philadelphia chromosome-positive cells,” Blood, vol. 86, no. 2, pp. 726–736, 1995.
- J. M. Goldman and J. V. Melo, “Mechanisms of disease: chronic myeloid leukemia—advances in biology and new approaches to treatment,” The New England Journal of Medicine, vol. 349, no. 15, pp. 1451–1464, 2003.
- X. Zhu, L. Wang, B. Zhang, J. Li, X. Dou, and R. C. Zhao, “TGF-β1-induced PI3K/Akt/NF-κB/MMP9 signalling pathway is activated in Philadelphia chromosome-positive chronic myeloid leukaemia hemangioblasts,” Journal of Biochemistry, vol. 149, no. 4, pp. 405–414, 2011.
- A. M. Martelli, M. Nyåkern, G. Tabellini et al., “Phosphoinositide 3-kinase/ Akt signaling pathway and its therapeutical implications for human acute myeloid leukemia,” Leukemia, vol. 20, no. 6, pp. 911–928, 2006.
- F. J. Giles and M. Albitar, “Mammalian target of rapamycin as a therapeutic target in leukemia,” Current Molecular Medicine, vol. 5, no. 7, pp. 653–661, 2005.
- Q. Xu, S. E. Simpson, T. J. Scialla, A. Bagg, and M. Carroll, “Survival of acute myeloid leukemia cells requires PI3 kinase activation,” Blood, vol. 102, no. 3, pp. 972–980, 2003.
- B. Calabretta and T. Skorski, “BCR/ABL regulation of PI-3 kinase activity,” Leukemia and Lymphoma, vol. 23, no. 5-6, pp. 473–476, 1996.
- A. Klejman, L. Rushen, A. Morrione, A. Slupianek, and T. Skorski, “Phosphatidylinositol-3 kinase inhibitors enhance the anti-leukemia effect of STI571,” Oncogene, vol. 21, no. 38, pp. 5868–5876, 2002.
- S. B. Marley, J. L. Lewis, H. Schneider, C. E. Rudd, and M. Y. Gordon, “Phosphatidylinositol-3 kinase inhibitors reproduce the selective antiproliferative effects of imatinib on chronic myeloid leukaemia progenitor cells,” British Journal of Haematology, vol. 125, no. 4, pp. 500–511, 2004.
- E. Weisberg, L. Banerji, R. D. Wright et al., “Potentiation of antileukemic therapies by the dual PI3K PDK-1 inhibitor, BAG956: effects on BCR-ABL and mutant FLT3-expressing cells,” Blood, vol. 111, no. 7, pp. 3723–3734, 2008.
- H. Lei and F. W. Quelle, “FOXO transcription factors enforce cell cycle checkpoints and promote survival of hematopoietic cells after DNA damage,” Molecular Cancer Research, vol. 7, no. 8, pp. 1294–1303, 2009.