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Fig. 8 | Journal of Experimental & Clinical Cancer Research

Fig. 8

From: Chidamide increases the sensitivity of refractory or relapsed acute myeloid leukemia cells to anthracyclines via regulation of the HDAC3 -AKT-P21-CDK2 signaling pathway

Fig. 8

Suppression of HDAC3 and AKT are required for chidamide induced anthracycline-resistant AML cells inhibition. HL60/ADR cells were treated with chidamide for 48 h and transfected with overexpressed HDAC3 plasmids or control plasmids. a CCK-8 assays were used to assess cell proliferation ability. b-c Cell cycle detection by flow cytometry. d Detection of apoptosis by flow cytometry. The expression of HDAC3 and AKT was measured by RT-PCR (e) and western blot analysis (f) HL60/ADR cells were treated with chidamide for 48 h and transfected with overexpressed AKT plasmids or control plasmids. g CCK-8 assays were used to assess cell proliferation ability. h-i Cell cycle detection by flow cytometry. j-k Detection of apoptosis by flow cytometry. The expression of HDAC3 and AKT was measured by RT-PCR (l) and western blot analysis (m). n Co-immunoprecipitation of AKT and HDAC3 were performed in 293 T cells. Data represents three independent experiments, data are expressed as mean values± S.D. (*P < 0.05, **P < 0.01, ***P < 0.001, NS: P > 0.05)

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