Abstract: Objective To investigate the effects of decitabine (DAC) combined with arsenic trioxide (ATO) on proliferation and apoptosis of AML cells and its underlying molecular mechanism. Methods AML cell lines were treated with DAC and ATO alone or in combination. CCK8 was used to detect cell viability;Compusyn software was used to analyze the synergistic effects of the combination treatment;Flow cytometry was applied to determine the apoptosis and cell cycle distribution;Western blot was applied to detect the expressions of poly (ADP-ribose) polymerase (PARP), c-PARP, phosphatidylinositol 3-kinase (PI3K), p-PI3K, protein kinase B (Akt) and p-Akt. Results DAC and ATO alone inhibited AML cell proliferation in a concentration-dependent manner. The combination of the two drugs significantly inhibited cell proliferation, induced apoptosis and cycle arrest of AML cells (P＜0.05). Combination therapy reduced the phosphorylation level of PI3K and Akt (P＜0.05). Conclusions DAC combined with ATO may have anti-AML effect by inhibiting PI3K/Akt pathway, which provides new theoretical basis of DAC+ATO strategy for AML.

Key words: decitabine, arsenic trioxide, acute myeloid leukemia, proliferation, apoptosis