Objective:To observe the reversion of multi-drug resistance by proteasome inhibitor bortezomib in K562/DNR cell line and to analyze the possible mechanism of reversion of multidrug-resistance.Methods:MTT method was used to determine the drug resistance of K562/DNR cells and the cellular toxicity of bortezomib.K562/DNR cells were cultured for 12 hours,24 hours and 36 hours with 100 μg/ml DNR only or plus 4 μg/L bortezomib.The expressions of NF-κB,IκB and P-gp of K562/DNR were detected with Western blot method,the activity of NF-κB was tested by ELISA method and the apoptosis rate was observed in each group respectively.Results:The IC50 of DNR on cells of K562/S and K562/DNR groups were 1.16 μg/ml and 50.43 μg/mL,respectively.The drug-resistant fold was 43.47.The IC10 of PS-341 on Cell strain K562/DNR was 4 μg/L.Therefore,4 μg/L was selected as the concentration for PS-341 to reverse drug-resistance in this study.DNR induced down-regulation of IκB expression,up-regulation of NF-κB and P-gp expression.After treatment with PS-341,a proteasome inhibitor,the IκB degradation was inhibited,IκB expression increased,NF-κB and P-gp expression decreased in a time dependent manner.Compared to DNR group,the NF-κB p65 activity of DNR+PS-341 group was decreased.Compared to corresponding DNR group,DNR induced apoptosis rate increases after addition of PS-341 in a time dependent manner.Conclusion:Proteasome inhibitor bortezomib can convert the leukemia cell drug resistance.The mechanism may be that bortezomib decreases the degradation of IκB and the expression of NF-κB and P-gp,therefore induces the apoptosis of multi-drug resistant cells. Objective: To observe the reversion of multi-drug resistance by proteasome inhibitor bortezomib in K562 / DNR cell line and to analyze the possible mechanism of reversion of multidrug-resistance. Methods: MTT method was used to determine the drug resistance of K562 / DNR cells and the cellular toxicity of bortezomib.K562 / DNR cells were cultured for 12 hours, 24 hours and 36 hours with 100 μg / ml DNR only or plus 4 μg / L bortezomib. The expressions of NF-κB, IκB and P-gp of K562 / DNR were detected with Western blot method, the activity of NF-κB was tested by ELISA method and the apoptosis rate was observed in each group respectively. Results: The IC50 of DNR on cells of K562 / S and K562 / DNR groups were 1.16 μg / ml and 50.43 μg / mL respectively. The drug-resistant fold was 43.47. The IC10 of PS-341 on Cell strain K562 / DNR was 4 μg / L. Therefore, 4 μg / L was selected as the concentration for PS-341 to reverse drug-resistance in this study. DNR induced down-regulation of IκB expression, up-regulation of NF -κB and P-gp expression. After treatment with PS-341, a proteasome inhibitor, the IκB degradation was inhibited, IκB expression increased, NF-κB and P-gp expression decreased in a time dependent manner. Compared to DNR group, the DNR induced apoptosis rate increases after addition of PS-341 in a time-dependent manner. Conclusion: Proteasome inhibitor bortezomib can convert the leukemia cell drug resistance The mechanism may be that bortezomib decreases the degradation of IκB and the expression of NF-κB and P-gp, therefore induces the apoptosis of multi-drug resistant cells.