MiR-155 promotes FLT3-ITD-induced myeloproliferative disease through inhibition of the interferon response.

ABSTRACT: FLT3-ITD⁺ acute myeloid leukemia (AML) accounts for ∼25% of all AML cases and is a subtype that carries a poor prognosis. microRNA-155 (miR-155) is specifically overexpressed in FLT3-ITD⁺ AML compared with FLT3 wild-type (FLT3-WT) AML and is critical for the growth of FLT3-ITD⁺ AML cells in vitro. However, miR-155's role in regulating FLT3-ITD-mediated disease in vivo remains unclear. In this study, we used a genetic mouse model to determine whether miR-155 influences the development of FLT3-ITD-induced myeloproliferative disease. Results indicate that miR-155 promotes FLT3-ITD-induced myeloid expansion in the bone marrow, spleen, and peripheral blood. Mechanistically, miR-155 increases proliferation of the hematopoietic stem and progenitor cell compartment

SUBMITTER: Wallace JA 

PROVIDER: S-EPMC5465836 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature