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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

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. 5

Molecular mechanisms of chidamide activity in HL60/ADR and patient-derived anthracycline-resistant AML cells. Anthracycline-resistant AML cells were treated with different concentrations of chidamide. Expression levels of HDAC3, AKT, P21 and CDK2 were measured using RT-PCR in HL60/ADR (a) and primary AML cells (b-c). d HL60/ADR and (e) primary AML cells were treated with chidamide and expression levels of HDAC3, P-AKT, AKT, P21, and CDK2 were measured by Western blot. The expression of HDAC3, AKT, P21, and CDK2 was measured by RT-PCR (f) and Western blot (g) in HL60/ADR cells after treated with a combination of chidamide and doxorubicin. RT-PCR analysis of HDAC3, AKT,CDK2 and P21 (h) and western blot analysis (i) in primary AML cells treated with combination therapy. GAPDH was used as the loading control. Data represents three independent experiments, and results are shown in the format, means ± S.D. (*P < 0.05, **P < 0.01, ***P < 0.001)

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