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. 2020 Dec 1;35(7):1933–1948. doi: 10.1038/s41375-020-01095-z

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — 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)).