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Cytoplasmatic compartmentalization by Bcr-Abl promotes TET2 loss-of-function in chronic myeloid leukemia
被引:17
作者:

Mancini, Manuela
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Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy

Veljkovic, Nevena
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Univ Belgrade, Ctr Multidisciplinary Res, Inst Nucl Sci, Belgrade, Serbia Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy

Leo, Elisa
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Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy

Aluigi, Michela
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Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy

Borsi, Enrica
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Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy

Galloni, Chiara
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Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy

Iacobucci, Ilaria
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Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy

Barbieri, Enza
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Univ Bologna, Dipartimento Sci Radiol & Istopatol, Ist Radioterapia Luigi Galvani, Sch Med, I-40138 Bologna, Italy Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy

Santucci, Maria Alessandra
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Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy
机构:
[1] Univ Bologna, Dipartimento Ematol & Sci Oncol Lorenzo & Ariosto, Sch Med, I-40138 Bologna, Italy
[2] Univ Belgrade, Ctr Multidisciplinary Res, Inst Nucl Sci, Belgrade, Serbia
[3] Univ Bologna, Dipartimento Sci Radiol & Istopatol, Ist Radioterapia Luigi Galvani, Sch Med, I-40138 Bologna, Italy
关键词:
CHRONIC MYELOID LEUKEMIA;
Bcr-Abl;
TET2;
BIM;
FoxO3a;
EPIGENETIC MODIFICATIONS;
ACUTE LYMPHOBLASTIC-LEUKEMIA;
HEMATOPOIETIC STEM-CELLS;
SELF-RENEWAL;
MLL;
BIM;
PROTEIN;
DNA;
5-METHYLCYTOSINE;
INHIBITOR;
HYDROXYLATION;
D O I:
10.1002/jcb.24154
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:
The loss-of-function of teneleven-translocation (TET) 2, a Fe2+-oxoglutarate-dependent dioxygenase catalyzing 5 methyl cytosine (5mC) conversion into 5-hydroxymethylcytosine (5hmC), contributes to the hematopoietic transformation in vivo. The aim of our study was to elucidate its role in the phenotype of chronic myeloid leukemia (CML), a myeloproliferative disease caused by the Bcr-Abl rearranged gene. We first confirmed TET2 interaction with the Bcr-Abl protein predicted by a Fourier-based bioinformatic method. Such interaction led to TET2 cytoplasmatic compartmentalization in a complex tethered by the fusion protein tyrosine kinase (TK) and encompassing the Forkhead box O3a (FoxO3a) transcription factor. We then focused the impact of TET2 loss-of-function on epigenetic transcriptional regulation of Bcl2-interacting mediator (BIM), a pro-apoptotic protein transcriptionally regulated by FoxO3a. BIM downregulation is a critical component of CML progenitor extended survival and is also involved in the disease resistance to imatinib (IM). Here we reported that TET2 release from Bcr-Abl protein following TK inhibition in response to IM triggers a chain of events including TET2 nuclear translocation, re-activation of its enzymatic function at 5mC and recruitment at the BIM promoter followed by BIM transcriptional induction. 5hmC increment following TET2 re-activation was associated with the reduction of histone H3 tri-methylation at lysine 9 (H3K9me3), which may contribute with DNA de-methylation reported elsewhere to recast a permissive epigenetic landscape for FoxO3a transcriptional activity. J. Cell. Biochem. 113: 27652774, 2012. (c) 2012 Wiley Periodicals, Inc.
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收藏
页码:2765 / 2774
页数:10
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Uppsala Univ, Rudbeck Lab, Dept Genet & Pathol, Uppsala, Sweden Vrije Univ Brussel, Dept Hematol & Immunol, B-1090 Brussels, Belgium

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Gemin X Biotechnol Inc, Montreal, PQ, Canada Emory Univ, Sch Med, Winship Canc Inst, Atlanta, GA 30322 USA

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de Mattos, SF
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h-index: 0
机构: Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Dept Canc Med, Canc Res UK Labs, London W12 0NN, England

Hassen, YAM
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h-index: 0
机构: Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Dept Canc Med, Canc Res UK Labs, London W12 0NN, England

Soeiro, I
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机构: Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Dept Canc Med, Canc Res UK Labs, London W12 0NN, England

Mufti, GJ
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机构: Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Dept Canc Med, Canc Res UK Labs, London W12 0NN, England

Thomas, NSB
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h-index: 0
机构: Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Dept Canc Med, Canc Res UK Labs, London W12 0NN, England

Medema, RH
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h-index: 0
机构: Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Dept Canc Med, Canc Res UK Labs, London W12 0NN, England

Lam, EWF
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h-index: 0
机构: Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Dept Canc Med, Canc Res UK Labs, London W12 0NN, England