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We found that miR-320a expression was reduced in K562 and in CML cancer stem cells. Moreover, we found that miR-320a inhibited K562 cell migration, invasion, proliferation and promoted apoptosis by targeting BCR\/ABL oncogene. As an upstream regulator of BCR\/ABL, miR-320a directly targets BCR\/ABL. The enhanced expression of miR-320a inhibited the phosphorylation of PI3K, AKT and NF-\u03baB; however, the expression of phosphorylated PI3K, AKT and NF-\u03baB were restored by the overexpression of BCR\/ABL. In K562, infected with miR-320a or transfected with SiBCR\/ABL, the protein levels of fibronectin, vimentin and N-cadherin were decreased, but the expression of E-cadherin was increased. The expression of mesenchymal markers in miR-320a-expressing cells was restored to normal levels by the restoration of BCR\/ABL expression. 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