197
Views
11
CrossRef citations to date
0
Altmetric
Original Articles: Research

Arsenic trioxide cooperates with all trans retinoic acid to enhance mitogen-activated protein kinase activation and differentiation in PML–RARα negative human myeloblastic leukemia cells

, , , , &
Pages 1-14 | Received 12 May 2010, Accepted 10 Jun 2010, Published online: 08 Jul 2010

References

  • Waxman S, Anderson KC. History of the development of arsenic derivatives in cancer therapy. Oncologist 2001;6:3–10.
  • Evens AM, Tallman MS, Gartenhaus RB. The potential of arsenic trioxide in the treatment of malignant disease: past, present, and future. Leuk Res 2004;28:891–900.
  • Wang ZY, Chen Z. Acute promyelocytic leukemia: from highly fatal to highly curable. Blood 2008;111:2505–2515.
  • Niu C, Yan H, Yu T, et al Studies on treatment of acute promyelocytic leukemia with arsenic trioxide: remission induction, follow-up, and molecular monitoring in 11 newly diagnosed and 47 relapsed acute promyelocytic leukemia patients. Blood 1999;94:3315–3324.
  • Shen ZX, Chen GQ, Ni JH, et al Use of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia (APL): II. Clinical efficacy and pharmacokinetics in relapsed patients. Blood 1997;89:3354–3360.
  • Mathews V, George B, Lakshmi KM, et al Single-agent arsenic trioxide in the treatment of newly diagnosed acute promyelocytic leukemia: durable remissions with minimal toxicity. Blood 2006;107:2627–2632.
  • Breitman T, Collins S, Keene B. Terminal differentiation of human promyelocytic leukemic cells in primary culture in response to retinoic acid. Blood 1981;57:1000–1004.
  • Huang M, Ye Y, Chen S, et al Use of all-trans retinoic acid in the treatment of acute promyelocytic leukemia. Blood 1988;72:567–572.
  • Asou N, Kishimoto Y, Kiyoi H, et al A randomized study with or without intensified maintenance chemo- therapy in patients with acute promyelocytic leukemia who have become negative for PML-RARalpha transcript after consolidation therapy: The Japan Adult Leukemia Study Group (JALSG) APL97 study. Blood 2007;110:59–66.
  • Shen ZX, Shi ZZ, Fang J, et al All-trans retinoic acid/As2O3 combination yields a high quality remission and survival in newly diagnosed acute promyelocytic leukemia. Proc Natl Acad Sci USA 2004;101:5328–5335.
  • Zhang XW, Yan XJ, Zhou ZR, et al Arsenic trioxide controls the fate of the PML–RARα oncoprotein by directly binding PML. Science 2010;328:240–243.
  • Yen A, Roberson MS, Varvayanis S, Lee AT. Retinoic acid induced mitogen-activated protein (MAP)/extracellular signal-regulated kinase (ERK) kinase-dependent MAP kinase activation needed to elicit HL-60 cell differentiation and growth arrest. Cancer Res 1998;58:3163–3172.
  • Wang J, Yen A. A MAPK-positive feedback mechanism for BLR1 signaling propels retinoic acid-triggered differentiation and cell cycle arrest. J Biol Chem 2008;283:4375–4386.
  • Perkins C, Kim C, Fang G, Bhalla K. Arsenic induces apoptosis of multidrug-resistant human myeloid leukemia cells that express Bcr-Abl or overexpress MDR, MRP, Bcl-2, or Bcl-xL. Blood 2000;95:1014–1022.
  • Herst P, Hesketh E, Ritchie D, Berridge M. Glycolytic metabolism confers resistance to combined all-trans retinoic acid and arsenic trioxide-induced apoptosis in HL60rho0 cells. Leuk Res 2008;32:327–333.
  • Jiang G, Albihn A, Tang T, Tian Z, Henriksson M. Role of Myc in differentiation and apoptosis in HL60 cells after exposure to arsenic trioxide or all-trans retinoic acid. Leuk Res 2008;32:297–307.
  • Chen GQ, Zhu J, Shi XG, et al In vitro studies on cellular and molecular mechanisms of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia: As2O3 induces NB4 cell apoptosis with downregulation of Bcl-2 expression and modulation of PML-RAR alpha/PML proteins. Blood 1996;88:1052–1061.
  • Fernandez C, Ramos AM, Sancho P, Amran D, de Blas E, Aller P. 12-O-Tetradecanoylphorbol-13-acetate may both potentiate and decrease the generation of apoptosis by the antileukemic agent arsenic trioxide in human promonocytic cells. J Biol Chem 2004;279:3877–3884.
  • Huang C, Ma W, Li J, Dong Z. Arsenic induces apoptosis through a c-Jun NH2-terminal kinase-dependent, p53-independent pathway. Cancer Res 1999;59:3053–3058.
  • Kishimoto H, Hoshino S, Ohori M, et al Molecular mechanism of human CD38 gene expression by retinoic acid identification of retinoic acid response element in the first intron. J Biol Chem 1998;273:15429–15434.
  • Shen M, Yen A. c-Cbl interacts with CD38 and promotes retinoic acid-induced differentiation and G0 arrest of human myeloblastic leukemia cells. Cancer Res 2008;68:8761–8769.
  • Reiterer G, Bunaciu RP, Smith JL, Yen A. Inhibiting the platelet derived growth factor receptor increases signs of retinoic acid syndrome in myeloid differentiated HL-60 cells. FEBS Lett 2008;582:2508–2514.
  • Shen M, Yen A. Nicotinamide cooperates with retinoic acid and 1,25-dihydroxyvitamin D3 to regulate cell differentiation and cell cycle arrest of human myeloblastic leukemia cells. Oncology 2009;76:91–100.
  • Muscarella DE, Rachlinski MK, Sotiriadis J, Bloom SE. contribution of gene-specific lesions, DNA-replication-associated damage, and subsequent transcriptional inhibition-mediated apoptosis in lymphoma cells. Exp Cell Res 1998;238:155–167.
  • Lamkin TJ, Chin V, Varvayanis S, et al Retinoic acid-induced CD38 expression in HL-60 myeloblastic leukemia cells regulates cell differentiation of viability depending on expression levels. J Cell Biochem 2006;97:1328–1338.
  • Shao W. Arsenic trioxide as an inducer of apoptosis and loss of PML/RAR alpha protein in acute promyelocytic leukemia cells. J Natl Cancer Inst 1998;90:124–133.
  • Jing Y, Dai J, Chalmers-Redman RME, Tatton WG, Waxman S. Arsenic trioxide selectively induces acute promyelocytic leukemia cell apoptosis via a hydrogen peroxide-dependent pathway. Blood 1999;94:2102–2111.
  • Davison K, Mann KK, Waxman S, Miller WH. JNK activation is a mediator of arsenic trioxide-induced apoptosis in acute promyelocytic leukemia cells. Blood 2004;103:3496–3502.
  • Dai J, Weinberg RS, Waxman S, Jing Y. Malignant cells can be sensitized to undergo growth inhibition and apoptosis by arsenic trioxide through modulation of the glutathione redox system. Blood 1999;93:268–277.
  • Ramos AM, Fernandez C, Amran D, Sancho P, de Blas E, Aller P. Pharmacologic inhibitors of PI3K/Akt potentiate the apoptotic action of the antileukemic drug arsenic trioxide via glutathione depletion and increased peroxide accumulation in myeloid leukemia cells. Blood 2005;105:4013–4020.
  • Chen GQ, Shi XG, Tang W, et al Use of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia (APL): I. As2O3 exerts dose-dependent dual effects on APL cells. Blood 1997;89:3345–3353.
  • Verma A, Mohindru M, Deb DK, et al Activation of Rac1 and the p38 mitogen-activated protein kinase pathway in response to arsenic trioxide. J Biol Chem 2002;277:44988–44995.
  • Zhao Q, Tao J, Zhu Q, et al Rapid induction of cAMP/ PKA pathway during retinoic acid-induced acute promyelocytic leukemia cell differentiation. Leukemia 2003;18:285–292.
  • Zheng PZ, Wang KK, Zhang QY, et al Systems analysis of transcriptome and proteome in retinoic acid/arsenic trioxide-induced cell differentiation/apoptosis of promyelocytic leukemia. Proc Natl Acad Sci USA 2005;102:7653–7658.
  • Zhu Q, Zhang JW, Zhu HQ, et al Synergic effects of arsenic trioxide and cAMP during acute promyelocytic leukemia cell maturation subtends a novel signaling cross-talk. Blood 2002;99:1014–1022.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.