MiR-302a sensitizes leukemia cells to etoposide by targeting Rad52.

miR-302a have been reported to participate in various physiological and pathological processes， however， a role for miR-302a in etoposide (VP-16) resistance of acute myeloid leukemia (AML) has not been reported. In this study， the aberrant expression of miR-302a was analyzed in patients with AML and in the AML HL-60 and U937 cell lines. Overexpression of miR-302a， by targeting the 3'UTR of Rad52， enhanced VP-16 sensitivity in the HL-60 and U937 cell. Accordingly， knockdown of Rad52 sensitized the HL-60 and U937 cells to VP-16-induced apoptosis and proliferation suppression. In addition， miR-302a enhanced the tumor-suppressive effect of VP-16 in a xenograft model of human HL-60 and U937 cell lines. Moreover， miR-302a repressed the AKT/Gsk3β/β-catenin pathway after Rad52 inhibition. Reintroduction of Rad52 reversed miR-302a-induced signaling suppression. The results of the present study demonstrated that miR-302a may be a target for the treatment of AML and a potential indicator of the therapeutic sensitivity of AML to VP-16.