Advertisement

 

 

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

MicroRNA-155 is a direct target of Meis1, but not a driver in acute myeloid leukemia.
Author Information (click to view)

Schneider E, Staffas A, Röhner L, Malmberg ED, Ashouri A, Krowiorz K, Pochert N, Miller C, Wei SY, Arabanian L, Buske C, Döhner H, Bullinger L, Fogelstrand L, Heuser M, Döhner K, Xiang P, Ruschmann J, Petriv OI, Heravi-Moussavi A, Hansen CL, Hirst M, Humphries RK, Rouhi A, Palmqvist L, Kuchenbauer F,


Schneider E, Staffas A, Röhner L, Malmberg ED, Ashouri A, Krowiorz K, Pochert N, Miller C, Wei SY, Arabanian L, Buske C, Döhner H, Bullinger L, Fogelstrand L, Heuser M, Döhner K, Xiang P, Ruschmann J, Petriv OI, Heravi-Moussavi A, Hansen CL, Hirst M, Humphries RK, Rouhi A, Palmqvist L, Kuchenbauer F, (click to view)

Schneider E, Staffas A, Röhner L, Malmberg ED, Ashouri A, Krowiorz K, Pochert N, Miller C, Wei SY, Arabanian L, Buske C, Döhner H, Bullinger L, Fogelstrand L, Heuser M, Döhner K, Xiang P, Ruschmann J, Petriv OI, Heravi-Moussavi A, Hansen CL, Hirst M, Humphries RK, Rouhi A, Palmqvist L, Kuchenbauer F,

Advertisement
Share on FacebookTweet about this on TwitterShare on LinkedIn

Haematologica 2017 12 07() pii haematol.2017.177485
Abstract

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.

Submit a Comment

Your email address will not be published. Required fields are marked *

3 × 3 =

[ HIDE/SHOW ]