BMI1 reprogrammes histone acetylation and enhances c-fos pathway via directly binding to Zmym3 in malignant myeloid progression

Journal of Cellular and Molecular Medicine

Volumn 18, Issue 6, 2014, Pages 1004-1017

  Shen, Hongjie ^a   Chen, Zixing ^a   Ding, Xin ^b   Qi, Xiaofei ^a   Cen, Jiannong ^a   Wang, Yuanyuan ^a   Yao, Li ^a   Chen, Yan ^a  

^a THE FIRST AFFILIATED HOSPITAL OF SOOCHOW UNIVERSITY   (China)

^b XUZHOU MEDICAL UNIVERSITY   (China)

Author keywords

Acetylation; BMI1; Chronic myeloid leukaemia; Myelodysplastic syndrome; ZMYM3

Indexed keywords

12-O-TETRADECANOYLPHORBOL-1,3-ACETATE; ANTIHISTAMINIC AGENT; BMI1 PROTEIN; BMI1 PROTEIN, HUMAN; BUTYRIC ACID; HISTONE; MESSENGER RNA; NUCLEAR PROTEIN; PHORBOL 13 ACETATE 12 MYRISTATE; PROTEIN BINDING; PROTEIN C FOS; ZMYM3 PROTEIN, HUMAN;

ACETYLATION; ADOLESCENT; ADULT; AGED; ANALOGS AND DERIVATIVES; APOPTOSIS; CASE CONTROL STUDY; CELL CULTURE; CELL DIFFERENTIATION; CELL PROLIFERATION; CHROMATIN IMMUNOPRECIPITATION; CHRONIC MYELOID LEUKEMIA; COMPARATIVE STUDY; DRUG EFFECTS; FEMALE; FLOW CYTOMETRY; GENE EXPRESSION REGULATION; GENETICS; HUMAN; MALE; METABOLISM; MIDDLE AGED; MYELODYSPLASTIC SYNDROME; PATHOLOGY; REAL TIME POLYMERASE CHAIN REACTION; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; VERY ELDERLY; WESTERN BLOTTING; YOUNG ADULT;

ACETYLATION; ADOLESCENT; ADULT; AGED; AGED, 80 AND OVER; APOPTOSIS; BLOTTING, WESTERN; BUTYRIC ACID; CASE-CONTROL STUDIES; CELL DIFFERENTIATION; CELL PROLIFERATION; CELLS, CULTURED; CHROMATIN IMMUNOPRECIPITATION; FEMALE; FLOW CYTOMETRY; GENE EXPRESSION REGULATION, NEOPLASTIC; HISTAMINE ANTAGONISTS; HISTONES; HUMANS; LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE; MALE; MIDDLE AGED; MYELODYSPLASTIC SYNDROMES; NUCLEAR PROTEINS; POLYCOMB REPRESSIVE COMPLEX 1; PROTEIN BINDING; PROTO-ONCOGENE PROTEINS C-FOS; REAL-TIME POLYMERASE CHAIN REACTION; REVERSE TRANSCRIPTASE POLYMERASE CHAIN REACTION; RNA, MESSENGER; TETRADECANOYLPHORBOL ACETATE; YOUNG ADULT;

EID: 84904742765     PISSN: 15821838     EISSN: 15824934     Source Type: Journal    
DOI: 10.1111/jcmm.12246     Document Type: Article

References (51)

1. Tefferi A, Vardiman JW. Myelodysplastic syndromes. N Engl J Med. 2009; 361: 1872-85.
2. Issa JP. The myelodysplastic syndrome as a prototypical epigenetic disease. Blood. 2013; 121: 3811-7.
3. Pang WW, Pluvinage JV, Price EA, et al. Hematopoietic stem cell and progenitor cell mechanisms in myelodysplastic syndromes. Proc Natl Acad Sci USA. 2013; 110: 3011-6.
4. Shannon K, Armstrong SA. Genetics, epigenetics, and leukemia. N Engl J Med. 2010; 363: 2460-1.
5. Costa D, Muñoz C, Carrió A, et al. Reciprocal translocations in myelodysplastic syndromes and chronic myelomonocytic leukemias: review of 5654 patients with an evaluable karyotype. Genes Chromosom Cancer. 2013; 52: 753-63.
6. Bejar R, Stevenson K, Abdel-Wahab O, et al. Clinical effect of point mutations in myelodysplastic syndromes. N Engl J Med. 2011; 364: 2496-506.
7. Wei Y, Gañán-Gómez I, Salazar-Dimicoli S, et al. Histone methylation in myelodysplastic syndromes. Epigenomics. 2011; 3: 193-205.
8. Ishibashi M, Tamura H, Ogata K. Disease progression mechanism in myelodysplastic syndromes: insight into the role of the microenvironment. Leuk Res. 2011; 35: 1449-52.
9. Aggarwal S, van de Loosdrecht AA, Alhan C, et al. Role of immune responses in the pathogenesis of low-risk MDS and high-risk MDS: implications for immunotherapy. Br J Haematol. 2011; 153: 568-81.
10. Agarwal A. MDS: roadblock to differentiation. Blood. 2012; 120: 1968-9.
11. Ito T. Stem cell maintenance and disease progression in chronic myeloid leukemia. Int J Hematol. 2013; 98: 641-7.
12. Skorski T. Chronic myeloid leukemia cells refractory/resistant to tyrosine kinase inhibitors are genetically unstable and may cause relapse and malignant progression to the terminal disease state. Leuk Lymphoma. 2011; 52: 23-9.
13. Tantiworawit A, Power MM, Barnett MJ, et al. Long-term follow-up of patients with chronic myeloid leukemia in chronic phase developing sudden blast phase on imatinib therapy. Leuk Lymphoma. 2012; 53: 1321-6.
14. Slupianek A, Falinski R, Znojek P, et al. BCR-ABL1 kinase inhibits uracil DNA glycosylase UNG2 to enhance oxidative DNA damage and stimulate genomic instability. Leukemia. 2013; 27: 629-34.
15. Roche-Lestienne C, Deluche L, Corm S, et al. RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance. Blood. 2008; 111: 3735-41.
16. Grossmann V, Kohlmann A, Zenger M, et al. A deep-sequencing study of chronic myeloid leukemia patients in blast crisis (BC-CML) detects mutations in 76.9% of cases. Leukemia. 2011; 25: 557-60.
17. Zhao LJ, Wang YY, Li G, et al. Functional features of RUNX1 mutants in acute transformation of chronic myeloid leukemia and their contribution to inducing murine full-blown leukemia. Blood. 2012; 119: 2873-82.
18. Makishima H, Jankowska AM, McDevitt MA, et al. CBL, CBLB, TET2, ASXL1, and IDH1/2 mutations and additional chromosomal aberrations constitute molecular events in chronic myelogenous leukemia. Blood. 2011; 117: e198-206.
19. Germing U, Lauseker M, Hildebrandt B, et al. Survival, prognostic factors and rates of leukemic transformation in 381 untreated patients with MDS and del(5q): a multicenter study. Leukemia. 2012; 26: 1286-92.
20. Lessard J, Sauvageau G. Bmi-1 determines the proliferative capacity of normal and leukaemic stem cells. Nature. 2003; 423: 255-60.
21. Agherbi H, Gaussmann-Wenger A, Verthuy C, et al. Polycomb mediated epigenetic silencing and replication timing at the INK4a/ARF locus during senescence. PLoS ONE. 2009; 4: e5622.
22. Meng S, Luo M, Sun H, et al. Identification and characterization of Bmi-1- responding element within the human p16 promoter. J Biol Chem. 2010; 285: 33219-29.
23. Mihara K, Chowdhury M, Nakaju N, et al. Bmi-1 is useful as a novel molecular marker for predicting progression of myelodysplastic syndrome and patient prognosis. Blood. 2006; 107: 305-8.
24. Mohty M, Yong AS, Szydlo RM, et al. The polycomb group BMI1 gene is a molecular marker for predicting prognosis of chronic myeloid leukemia. Blood. 2007; 110: 380-3.
25. Kovitz C, Kantarjian H, Garcia-Manero G, et al. Myelodysplastic syndromes and acute leukemia developing after imatinib mesylate therapy for chronic myeloid leukemia. Blood. 2006; 108: 2811-3.
26. Meggendorfer M, Bacher U, Alpermann T, et al. SETBP1 mutations occur in 9% of MDS/MPN and in 4% of MPN cases are strongly associated with atypical CML, monosomy 7, isochromosome i(17)(q10), ASXL1 and CBL mutations. Leukemia. 2013; 27: 1852-60.
27. Yuan J, Takeuchi M, Negishi M, et al. Bmi1 is essential for leukemic reprogramming of myeloid progenitor cells. Leukemia. 2011; 25: 1335-43.
28. Rizo A, Horton SJ, Olthof S, et al. BMI1 collaborates with BCR-ABL in leukemic transformation of human CD34+ cells. Blood. 2010; 116: 4621-30.
29. Boukarabila H, Saurin AJ, Batsché E, et al. The PRC1 Polycomb group complex interacts with PLZF/RARA to mediate leukemic transformation. Genes Dev. 2009; 23: 1195-206.
30. Harada Y, Harada H. Molecular pathways mediating MDS/AML with focus on AML1/RUNX1 point mutations. J Cell Physiol. 2009; 220: 16-20.
31. Harada Y, Inoue D, Ding Y, et al. RUNX1/AML1 mutant collaborates with BMI1 overexpression in the development of human and murine myelodysplastic syndromes. Blood. 2013; 121: 3434-46.
32. Waldron T, De Dominici M, Soliera AR, et al. c-Myb and its target Bmi1 are required for p190 BCR/ABL leukemogenesis in mouse and human cells. Leukemia. 2012; 26: 644-53.
33. Drexler HG, Dirks WG, Macleod RA. Many are called MDS cell lines: one is chosen. Leuk Res. 2009; 33: 1011-6.
34. Smith LL, Yeung J, Zeisig BB, et al. Functional crosstalk between Bmi1 and MLL/Hoxa9 axis in establishment of normal hematopoietic and leukemic stem cells. Cell Stem Cell. 2011; 8: 649-62.
35. Della Porta MG. Prognosis of secondary acute myeloid leukemia. Leuk Res. 2013; 37: 857-8.
36. Milosevic JD, Puda A, Malcovati L, et al. Clinical significance of genetic aberrations in secondary acute myeloid leukemia. Am J Hematol. 2012; 87: 1010-6.
37. Kulasekararaj AG, Smith AE, Mian SA, et al. TP53 mutations in myelodysplastic syndrome are strongly correlated with aberrations of chromosome 5, and correlate with adverse prognosis. Br J Haematol. 2013; 160: 660-72.
38. Wall M, Rayeroux KC, MacKinnon RN, et al. ETV6 deletion is a common additional abnormality in patients with myelodysplastic syndromes or acute myeloid leukemia and monosomy 7. Haematologica. 2012; 97: 1933-6.
39. Yilmaz OH, Valdez R, Theisen BK, et al. Pten dependence distinguishes haematopoietic stem cells from leukaemia-initiating cells. Nature. 2006; 441: 475-82.
40. Peng C, Chen Y, Yang Z, et al. PTEN is a tumor suppressor in CML stem cells and BCR-ABL-induced leukemias in mice. Blood. 2010; 115: 626-35.
41. Fan C, He L, Kapoor A, et al. PTEN inhibits BMI1 function independently of its phosphatase activity. Mol Cancer. 2009; 8: 98.
42. Ooi L, Wood IC. Chromatin crosstalk in development and disease: lessons from REST. Nature Rev Genet. 2007; 8: 544-54.
43. Jung JW, Lee S, Seo MS, et al. Histone deacetylase controls adult stem cell aging by balancing the expression of polycomb genes and jumonji domain containing 3. Cell Mol Life Sci. 2010; 67: 1165-76.
44. Sustáčková G, Kozubek S, Stixová L, et al. Acetylation-dependent nuclear arrangement and recruitment of BMI1 protein to UV-damaged chromatin. J Cell Physiol. 2012; 227: 1838-50.
45. Hakimi MA, Dong Y, Lane WS, et al. A candidate X-linked mental retardation gene is a component of a new family of histone deacetylase-containing complexes. J Biol Chem. 2003; 278: 7234-9.
46. Lee MG, Wynder C, Cooch N, et al. An essential role for CoREST in nucleosomal histone 3 lysine 4 demethylation. Nature. 2005; 437: 432-5.
47. Vaquero A, Scher M, Reinberg D. Biochemistry of multiprotein HDAC complexes. In: Verdin E, editor. Cancer drug discovery and development, Histone deacetylases: transcriptional regulation and other cellular functions. New Jersey: Humana Press Inc; 2006. p. 23-60.
48. Pasini D, Malatesta M, Jung HR, et al. Characterization of an antagonistic switch between histone H3 lysine 27 methylation and acetylation in the transcriptional regulation of Polycomb group target genes. Nucleic Acids Res. 2010; 38: 4958-69.
49. Chen KC, Liu WH, Chang LS. Suppression of ERK signaling evokes autocrine Fas-mediated death in arachidonic acid-treated human chronic myeloid leukemia K562 cells. J Cell Physiol. 2010; 222: 625-34.
50. Waring P, Müllbacher A. Cell death induced by the Fas/Fas ligand pathway and its role in pathology. Immunol Cell Biol. 1999; 77: 312-7.
51. Kolonics A, Apáti A, Nahajevszky S, et al. Unregulated activation of STAT-5, ERK1/2 and c-Fos may contribute to the phenotypic transformation from myelodysplastic syndrome to acute leukaemia. Haematologia. 2001; 31: 125-38.