摘要

We have shown that inhibition of WT1/+17AA protein expression following transfection with a vector-based small interfering RNA expression construct in K562 cell lines, leads to a decrease in MDR1 and P-glycoprotein levels, accumulation of Rh123, and enhancement of the doxorubicin cytotoxicity. Our findings suggest that WT1/+17AA exerts its oncogenic function by modulating multidrug resistance in leukemia cells.