Fig. 7. miR-10a regulates cell cycle arrest and apoptosis.

a Subsequent to the repression of autophagy and cell cycle arrest observed in miR-10a-inhibited cells in response to Nutlin-3a and cytarabine treatment, cells became apoptotic. These pro-apoptotic effects could be recapitulated in the absence of miR-10a inhibition by knocking down CDKN1a expression, or overexpressing RB1CC1. b, c NPM1^wt primary AML specimens with high (n = 4) or low (n = 4) endogenous miR-10 expression (shown on right Y-axis of plot) were treated with a low (IC₂₅) does of Nutlin-3a, cytarabine, or Nutlin-3a+Cytarabine. Those samples with low miR-10a expression exhibited significantly higher levels of apoptosis (as measured by Annexin-V positivity (b)) and had significantly fewer cells arrested (c) in response to drugs compared to specimens with high miR-10a expression. (*p < 0.05, **p < 0.01; ***p < 0.001 by Student’s T test with error bars representing SD (3–6 replicates per experiment)).