217
Views
4
CrossRef citations to date
0
Altmetric
Original Articles: Research

Ecotropic viral integration site I regulates alpha1, 6-fucosyl transferase expression and blocks erythropoiesis in chronic myeloid leukemia

, , , , , , & show all
Pages 1941-1947 | Received 16 Aug 2016, Accepted 19 Nov 2016, Published online: 14 Dec 2016

References

  • Jacquel A, Herrant M, Legros L, et al. Imatinib induces mitochondria-dependent apoptosis of the Bcr-Abl-positive K562 cell line and its differentiation toward the erythroid lineage. FASEB J. 2003;17:2160–2162.
  • Mitelman F. The cytogenetic scenario of chronic myeloid leukemia. Leuk Lymphoma. 1993;11:11–15.
  • Gordon MY, Goldman JM. Cellular and molecular mechanisms in chronic myeloid leukaemia: biology and treatment. Br J Haematol. 1996;95:10–20.
  • Kelly LM, Gilliland DG. Genetics of myeloid leukemias. Annu Rev Genomics Hum Genet. 2002;3:179–198.
  • Gilliland DG, Tallman MS. Focus on acute leukemias. Cancer Cell. 2002;1:417–420.
  • Calabretta B, Perrotti D. The biology of CML blast crisis. Blood. 2004;103:4010–4022.
  • Ogawa S, Kurokawa M, Tanaka T, et al. Increased Evi-1 expression is frequently observed in blastic crisis of chronic myelocytic leukemia. Leukemia. 1996;10:788–794.
  • Russell M, Thompson F, Spier C, et al. Expression of the EVI1 gene in chronic myelogenous leukemia in blast crisis. Leukemia. 1993;7:1654–1657.
  • Ohyashiki JH, Ohyashiki K, Shimamoto T, et al. Ecotropic virus integration site-1 gene preferentially expressed in post-myelodysplasia acute myeloid leukemia: possible association with GATA-1, GATA-2, and stem cell leukemia gene expression. Blood. 1995;85:3713–3718.
  • Daghistani M, Marin D, Khorashad JS, et al. EVI-1 oncogene expression predicts survival in chronic-phase CML patients resistant to imatinib treated with second-generation tyrosine kinase inhibitors. Blood. 2010;116:6014–6017.
  • Sato T, Goyama S, Kataoka K, et al. Evi1 defines leukemia-initiating capacity and tyrosine kinase inhibitor resistance in chronic myeloid leukemia. Oncogene. 2014;33:5028–5038.
  • Paquette RL, Nicoll J, Chalukya M, et al. Frequent EVI1 translocations in myeloid blast crisis CML that evolves through tyrosine kinase inhibitors. Cancer Genet. 2011;204:392–397.
  • Buonamici S, Li D, Chi Y, et al. EVI1 induces myelodysplastic syndrome in mice. J Clin Investig. 2004;114:713–719.
  • Louz D, van den Broek M, Verbakel S, et al. Erythroid defects and increased retrovirally-induced tumor formation in Evi1 transgenic mice. Leukemia. 2000;14:1876–1884.
  • Laricchia-Robbio L, Fazzina R, Li D, et al. Point mutations in two EVI1 Zn fingers abolish EVI1-GATA1 interaction and allow erythroid differentiation of murine bone marrow cells. Mol Cell Biol. 2006;26:7658–7666.
  • Osumi D, Takahashi M, Miyoshi E, et al. Core fucosylation of E-cadherin enhances cell-cell adhesion in human colon carcinoma WiDr cells. Cancer Sci. 2009;100:888–895.
  • Ito Y, Miyauchi A, Yoshida H, et al. Expression of alpha1,6-fucosyltransferase (FUT8) in papillary carcinoma of the thyroid: its linkage to biological aggressiveness and anaplastic transformation. Cancer Lett. 2003;200:167–172.
  • Kawamoto S, Moriwaki K, Nakagawa T, et al. Overexpression of α1,6-fucosyltransferase in hepatoma enhances expression of Golgi phosphoprotein 2 in a fucosylation-independent manner. Int J Oncol. 2011;39:203–208.
  • Chen CY, Jan YH, Juan YH, et al. Fucosyltransferase 8 as a functional regulator of nonsmall cell lung cancer. Proc Natl Acad Sci USA. 2013;110:630–635.
  • Wang X, Chen J, Li QK, et al. Overexpression of α (1,6) fucosyltransferase associated with aggressive prostate cancer. Glycobiology. 2014;24:935–944.
  • Honma R, Kinoshita I, Miyoshi E, et al. Expression of fucosyltransferase 8 is associated with an unfavorable clinical outcome in non-small cell lung cancers. Oncology. 2015;88:298–308.
  • Sasaki H, Toda T, Furukawa T, et al. α-1,6-Fucosyltransferase (FUT8) inhibits hemoglobin production during differentiation of murine and K562 human erythroleukemia cells. J Biol Chem. 2013;288:16839–16847.
  • Kustikova OS, Schwarzer A, Stahlhut M, et al. Activation of Evi1 inhibits cell cycle progression and differentiation of hematopoietic progenitor cells. Leukemia. 2013;27:1127–1138.
  • Bard-Chapeau EA, Jeyakani J, Kok CH, et al. Ecotropic viral integration site 1 (EVI1) regulates multiple cellular processes important for cancer and is a synergistic partner for FOS protein in invasive tumors. Proc Natl Acad Sci USA. 2012;109:2168–2173.
  • Radich JP, Dai H, Mao M, et al. Gene expression changes associated with progression and response in chronic myeloid leukemia. Proc Natl Acad Sci USA. 2006;103:2794–2799.
  • Kreider BL, Orkin SH, Ihle JN. Loss of erythropoietin responsiveness in erythroid progenitors due to expression of the Evi-1 myeloid-transforming gene. Proc Natl Acad Sci USA. 1993;90:6454–6458.
  • Belhacène N, Maulon L, Guérin S, et al. Differential expression of the Kell blood group and CD10 antigens: two related membrane metallopeptidases during differentiation of K562 cells by phorbol ester and hemin. FASEB J. 1998;12:531–539.
  • Racke FK, Lewandowska K, Goueli S, et al. Sustained activation of the extracellular signal-regulated kinase/mitogen-activated protein kinase pathway is required for megakaryocytic differentiation of K562 cells. J Biol Chem. 1997;272:23366–23370.
  • Tokunaga M, Ezoe S, Tanaka H, et al. BCR-ABL but not JAK2 V617F inhibits erythropoiesis through the Ras signal by inducing p21CIP1/WAF1. Glycobiology. 2010;285:31774–31782.
  • Meshkini A, Yazdanparast R. Regulation of p38, PKC/Foxo3a/p73 signaling network by GTP during erythroid differentiation in chronic myelogenous leukemia. Cell Biochem Biophys. 2013;67:675–687.

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.