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Down-regulation of WT1/+17AA gene expression using RNAi and modulating leukemia cell chemotherapy resistance

^* Department of Oncology, the Affiliated of People’s Hospital, Jiangsu University, Zhenjiang, Jiangsu, China
^° Central Laboratory of Experimental Hematology, the Affiliated of People’s Hospital of Jiangsu University, Zhenjing, Jiangsu, China

Correspondence: Professor Wenlin Xu, the Affiliated of People’s Hospital of Jiangsu University, 8 Dianli Road, Zhenjiang, Jiangsu 212002, P.R.China. Phone: international +86.511.5246930. Fax: international +86.511.5234387. E-mail: XWL0806{at}163.com

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.

Key words: WT1, isoform, RNA interference, multidrug resistance, P-glycoprotein, leukemia cell, K562, K562/A02.