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. 2020 Dec 9;39:278. doi: 10.1186/s13046-020-01792-8

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — HL60/ADR, THP-1/ADR and patient-derived anthracycline-resistant AML cells are sensitive to either chidamide monotherapy or combination therapy of chidamide + doxorubicin. CCK-8 assays were used to assess the abilities of HL60/ADR (a), THP-1/ADR (b) and patient-derived cells (c) to proliferate. HL60/ADR G1 phase (d) and proportion of S phase (e) in response to incubation with chidamide were measured using flow cytometry. f-g are representatives of flow cytometry (Annexin V/PI) for detection of apoptosis. The cell viability of (h) HL60/ADR and (i) patients-derived primary AML cells treated by combination therapy were measured with CCK-8 assays. HDAC activity of anthracycline-resistant AML cells which were treated with chidamide (j). Data represents three independent experiments, results are shown in the format, mean ± S.D. (*P < 0.05, **P < 0.01, ***P < 0.001, NS: P > 0.05)