miR196b-/- DNMT3A-mutant AML [RNA-seq]

microRNA (miRNA or miR) are aberrantly expressed in acute myeloid leukemia (AML), and clinically may have diagnostic, prognostic, and therapeutic value. We identify miR-196b, is overexpressed in high-risk subset of DNMT3A-mutant AML and its activity is important to maintain a differentiation block and limit innate immune signaling pathways in AML. We interrogated previously published experimentally defined and computationally predicated miR-196b targets compared with genes differentially expressed in miR-196b-/-Dnmt3a/Flt3ITD AML versus Dnmt3a/Flt3ITD AML. This identified that miR-196b regulates Pou2f1 and Pou2f2 (Oct1 and Oct2) in Dnmt3a/Flt3-mutant AML. To identify the gene expression and pathway changes associated with murine Dnmt3a/Flt3ITD-mutant leukemia cells with and without miR-196b. n=3 independent AML harvested from different miR-196b-/-Dnmt3a/Flt3ITD mice. AML cells were enriched for cKit prior to RNA isolation. Dnmt3a/Flt3ITD AML controls (n=3) were previously published PMID:27016502 and can be found under GSE77849.