GSE167571
R848 treated 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 demonstrating that miR-196b regulates Toll-like Receptor Signaling. This work uncovered that miR-196b represses TLR7/8 activation and innate immune signaling in AML and that TLR7/8 activates a Stat1 transcriptional response associated with induced co-stimulatory molecule expression on the surface of AML-derived monocytes and dendritic-like cells. Overall design: To identify the gene expression and pathway changes assoicated with Resiquimod (R848) treatment in murine Dnmt3a/Flt3ITD-mutant leukemia cells.