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MicroRNA-155 is a direct target of Meis1, but not a driver in acute myeloid leukemia.

Journal article
Authors Edith Schneider
Anna Staffas
Linda Röhner
Erik Malmberg
Arghavan Ashouri
Kathrin Krowiorz
Nicole Pochert
Christina Miller
Yuan Wei
Laleh S. Arabanian
Christian Buske
Hartmut Döhner
Lars Bullinger
Linda Fogelstrand
Michael Heuser
Konstanze Döhner
Ping Xiang
Jens Ruschmann
Oleh I Petriv
Alireza Heravi-Moussavi
Carl L Hansen
Martin Hirst
R Keith Humphries
Arefeh Rouhi
Lars Palmqvist
Florian Kuchenbauer
Published in Haematologica
Volume 103
Pages 246-255
ISSN 1592-8721
Publication year 2018
Published at Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages 246-255
Language en
Links dx.doi.org/10.3324/haematol.2017.17...
Subject categories Molecular medicine (genetics and pathology), Molecular medicine, Hematology


MicroRNA-155 (miR-155) is one of the first described oncogenic miRNAs. Although multiple direct targets of miR-155 have been identified, it is not clear how it contributes to the pathogenesis of acute myeloid leukemia. We found miR-155 to be a direct target of Meis1 in murine Hoxa9/Meis1 induced acute myeloid leukemia. The additional overexpression of miR 155 accelerated the formation of acute myeloid leukemia in Hoxa9 as well as in Hoxa9/Meis1 cells in vivo. However, in the absence or after the removal of miR-155, leukemia onset and progression were unaffected. Although, miR-155 accelerated growth and homing as well as impaired differentiation, our data underscore the pathophysiological relevance of miR 155 as an accelerator rather than a driver of leukemogenesis. This further highlights the complexity of the oncogenic program of Meis1 to compensate for the loss of a potent oncogene such as miR-155. These findings are highly relevant to current and developing approaches for targeting miR-155 in acute myeloid leukemia.

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