MicroRNA 29b functions in acute myeloid leukemia

被引：358

作者：

Garzon, Ramiro ^{[2
]}

Heaphy, Catherine E. A. ^{[2
]}

Havelange, Violaine ^{[1
]}

Fabbri, Muller ^{[1
]}

Volinia, Stefano ^{[1
]}

Tsao, Twee ^{[3
]}

Zanesi, Nicola ^{[1
]}

Kornblau, Steven M. ^{[3
]}

Marcucci, Guido ^{[2
]}

Calin, George A. ^{[4
]}

Andreeff, Michael ^{[3
]}

Croce, Carlo M. ^{[1
]}

机构：

[1] Ohio State Univ, Ctr Comprehens Canc, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA

[2] Ohio State Univ, Dept Med, Div Hematol & Oncol, Columbus, OH 43210 USA

[3] Univ Texas MD Anderson Canc Ctr, Dept Blood & Bone Marrow Transplantat, Sect Mol Hematol & Therapy, Houston, TX 77030 USA

[4] Univ Texas MD Anderson Canc Ctr, Dept Expt Therapeut, Houston, TX 77030 USA

来源：

BLOOD | 2009年 / 114卷 / 26期

基金：

美国国家卫生研究院;

关键词：

LUNG-CANCER; EXPRESSION; SIGNATURE; MCL-1; PROGNOSIS; REVEALS; MIR-29; FAMILY; TIME;

D O I：

10.1182/blood-2009-03-211938

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

MicroRNAs (miRNAs) are associated with cytogenetics and molecular subtypes of acute myelogeneous leukemia (AML), but their impact on AML pathogenesis is poorly understood. We have previously shown that miR-29b expression is deregulated in primary AML blasts. In this work, we investigated the functional role of miR-29b in leukemogenesis. Restoration of miR-29b in AML cell lines and primary samples induces apoptosis and dramatically reduces tumorigenicity in a xenograft leukemia model. Transcriptome analysis after ectopic transfection of synthetic miR-29b into leukemia cells indicates that miR-29b target apoptosis, cell cycle, and proliferation pathways. A significant enrichment for apoptosis genes, including MCL-1, was found among the mRNAs inversely correlated with miR-29b expression in 45 primary AML samples. Together, the data support a tumor suppressor role for miR-29 and provide a rationale for the use of synthetic miR-29b oligonucleotides as a novel strategy to improve treatment response in AML. (Blood. 2009; 114: 5331-5341)

引用

页码：5331 / 5341

页数：11

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