【Abstract】 Objective To investigate the effects of FLT3-ITD mutation on the development of human acute promyelocytic leukemia and its mechanism. Methods The FLT3-ITD mutation in human acute promyelocytic leukemia cell （NB4） were detected by PCR. The cell morphological changes in NB4 cells after FLT3-ITD mutation were observed by high-times optic microscope. Cell invasion was determined using in vitro scratch test. The relative expression of E-cad, crSMA, Vi, FN, TGF-p and Smad2 in NB4 cells after FLT3-ITD mutation were processed and analyzed by qRT-PCR and Western blotting. Results The NB4 cells demonstrated an elongated and spindle-shaped morphology after FLT3-ITD mutation. The invasion capacity in NB4 cells after FLT3-ITD mutation was significantly higher than that in blank control group. After FLT3-ITD mutation, the relative mRNA and protein expression levels of crSMA, Vi and FN in VSMC cells were significantly higher than that in blank control group （P all＜O.05） and the relative mRNA and protein expression levels of E-cad were significantly lower than that in blank control group （P all＜O.05）. The relative mRNA and protein expression levels of TGF-p and Smad2 in NB4 cells after FLT3-ITD mutation were significantly higher than that in blank control group（P all＜O.05）. The expression of Smad2, E-cad, alpha-SMA, Vi and FN in FLT3-ITD mutant group and non-mutant group decreased significantly after TGF-p silencing （P＜0.05） , while the expression of Smad2, E-cad, crSMA, Vi and FN in FLT3-ITD mutant group had no significant difference compared with non-mutant group （P〉0.05）. Conclusion FLT3-ITD mutation promotes the epithelial-mesenchymal transition process through the promotion of TGF-p production in NB4 cells. FLT3-ITD may be a novel therapeutic target of acute promyelocytic leukemia.