Differential and common leukemogenic potentials of multiple NUP98-Hox fusion proteins alone or with Meis1

被引:80
作者
Pineault, N
Abramovich, C
Ohta, H
Humphries, RK
机构
[1] British Columbia Canc Agcy, Terry Fox Lab, Vancouver, BC V5Z 1L3, Canada
[2] Univ British Columbia, Dept Med, Vancouver, BC V5Z 4E3, Canada
关键词
D O I
10.1128/MCB.24.5.1907-1917.2004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
NUP98-Hox fusion genes are newly identified oncogenes isolated in myeloid leukemias. Intriguingly, only Abd-B Hox genes have been reported as fusion partners, indicating that they may have unique overlapping leukemogenic properties. To address this hypothesis, we engineered novel NUP98 fusions with Hox genes not previously identified as fusion partners: the Abd-B-like gene HOXA10 and two Antennepedia-like genes, HOXB3 and HOXB4. Notably, NUP98-HOXA10 and NUP98-HOXB3 but not NUP98-HOXB4 induced leukemia in a murine transplant model, which is consistent with the reported leukemogenic potential ability of HOXA10 and HOXB3 but not HOXB4. Thus, the ability of Hox genes to induce leukemia as NUP98 fusion partners, although apparently redundant for Abd-B-like activity, is not restricted to this group, but rather is determined by the intrinsic leukemogenic potential of the Hox partner. We also show that the potent leukemogenic activity of Abd-B-like Hox genes is correlated with their strong ability to block hematopoietic differentiation. Conversely, coexpression of the Hox cofactor Meis1 alleviated the requirement of a strong intrinsic Hox-transforming potential to induce leukemia. Our results support a model in which many if not all Hox genes can be leukemogenic and point to striking functional overlap not previously appreciated, presumably reflecting common regulated pathways.
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页码:1907 / 1917
页数:11
相关论文
共 40 条
[1]   HOXB4-induced expansion of adult hematopoietic stem cells ex vivo [J].
Antonchuk, J ;
Sauvageau, G ;
Humphries, RK .
CELL, 2002, 109 (01) :39-45
[2]   Reduced proliferative capacity of hematopoietic stem cells deficient in hoxb3 and hoxb4 [J].
Björnsson, JM ;
Larsson, N ;
Brun, ACM ;
Magnusson, M ;
Andersson, E ;
Lundström, P ;
Larsson, J ;
Repetowska, E ;
Ehinger, M ;
Humphries, RK ;
Karlsson, S .
MOLECULAR AND CELLULAR BIOLOGY, 2003, 23 (11) :3872-3883
[3]   The t(7;11)(p15;p15) translocation in acute myeloid leukaemia fuses the genes for nucleoporin NUP98 and class I homeoprotein HOXA9 [J].
Borrow, J ;
Shearman, AM ;
Stanton, VP ;
Becher, R ;
Collins, T ;
Williams, AJ ;
Dube, I ;
Katz, F ;
Kwong, YL ;
Morris, C ;
Ohyashiki, K ;
Toyama, K ;
Rowley, J ;
Housman, DE .
NATURE GENETICS, 1996, 12 (02) :159-167
[4]   Overexpression of HOXA10 perturbs human lymphomyelopoiesis in vitro and in vivo [J].
Buske, C ;
Feuring-Buske, M ;
Antonchuk, J ;
Rosten, P ;
Hogge, DE ;
Eaves, CJ ;
Humphries, RK .
BLOOD, 2001, 97 (08) :2286-2292
[5]   Nup98-HoxA9 immortalizes myeloid progenitors, enforces expression of Hoxa9, Hoxa7 and Meis1, and alters cytokine-specific responses in a manner similar to that induced by retroviral co-expression of Hoxa9 and Meis1 [J].
Calvo, KR ;
Sykes, DB ;
Pasillas, MP ;
Kamps, MP .
ONCOGENE, 2002, 21 (27) :4247-4256
[6]   Meis1a suppresses differentiation by G-CSF and promotes proliferation by SCF: Potential mechanisms of cooperativity with Hoxa9 in myeloid leukemia [J].
Calvo, KR ;
Knoepfler, PS ;
Sykes, DB ;
Pasillas, MP ;
Kamps, MP .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (23) :13120-13125
[7]   Hoxa9 immortalizes a granulocyte-macrophage colony-stimulating factor-dependent promyelocyte capable of biphenotypic differentiation to neutrophils or macrophages, independent of enforced Meis expression [J].
Calvo, KR ;
Sykes, DB ;
Pasillas, M ;
Kamps, MP .
MOLECULAR AND CELLULAR BIOLOGY, 2000, 20 (09) :3274-3285
[8]   The role of MLL in hematopoiesis and leukemia [J].
Ernst, P ;
Wang, J ;
Korsmeyer, SJ .
CURRENT OPINION IN HEMATOLOGY, 2002, 9 (04) :282-287
[9]   Single-translocation and double-chimeric transcripts:: detection of NUP98-HOXA9 in myeloid leukemias with HOXA11 or HOXA13 breaks of the chromosomal translocation t(7;11)(p15;p15) [J].
Fujino, T ;
Suzuki, A ;
Ito, Y ;
Ohyashiki, K ;
Hatano, Y ;
Miura, I ;
Nakamura, T .
BLOOD, 2002, 99 (04) :1428-1433
[10]  
Goff DJ, 1997, DEVELOPMENT, V124, P627