Abstract: Objective To investigate the effect of artesunate inhibiting the expression of FOXP3 on proliferation, apoptosis and multidrug resistance of adriamycin (ADR) -resistant K562/ADR cells in chronic myeloid leukemia (CML), and to explore its mechanism. Methods The expressions of FOXP3 mRNA in K562 and K562/ADR cells were detected by real-time PCR. The expressions of FOXP3 proteins in K562 and K562/ADR cells were detected by Western blot assay. The K562/ADR cells were treated with different concentrations of artesunate (2.5, 5.0, 7.5, 10.0 and 12.5 mg/L) for 24 h. The toxicities of different concentrations of artesunate to K562/ADR cells were detected by CCK-8 assay, and the non-cytotoxic concentrations were screened. The expressions of FOXP3 mRNA and proteins in K562/ADR cells treated by non-cytotoxic concentration of artesunate were detected by RT-PCR and Western blot assay. The changes of toxicities of ADR in K562/ ADR cells were detected by CCK-8 assay. The average fluorescence intensities of ADR were detected by FCM assay. Results The expressions of FOXP3 were higher in K562/ADR cells than those in K562 cells. The mRNA and proteins expressions of FOXP3 were significantly lower in 2.5 mg/L group, 5 mg/L group and 7.5 mg/L group than those in the control group. The toxicities and concentrations of ADR were increased in K562/ADR cells treated by artesunate (both P＜0.05). Conclusion FOXP3 gene is highly expressed in adriamycin-resistant K562/ADR cells in CML. Artesunate can increase the concentrations of ADR and reverse multidrug resistance in K562/ADR cells by inhibiting the expression of FOXP3 in a dose-dependent manner.

Key words: drug resistance, neoplasm, leukemia, myeloid, K562 cells, FOXP3, Artesunate, multidug resistance