OBJECTIVE： To study the effects of protein kinase B inhibitor CCT128930 on the apoptosis and autophagy of human osteosarcoma U2-OS cells. METHODS： U2-OS cells were cultured in vitro， and the apoptosis of U2-OS cell was observed after treated with 0 （blank control， similarly hereinafter）， 10 and 20 μmol/L CCT128930 for 24 h. After treated with 0， 5， 10 and 20 μmol/L CCT128930 for 24 h， the protein expression of Caspase-3， Caspase-8， Caspase-9 and Caspase cutting substrate PARP， the proportion of autophagy-related protein LC3-Ⅱ/LC3-Ⅰ were detected by Western blot method. Plasmid GFP-LC3 transfected U2-OS cells； after treated with 0， 5 and 10 μmol/L CCT128930 for 24 h， immunofluorescence was used to detect the expression of GFP-LC3 protein. MTT assay and Western blot assay were used to detect the viability， the expression of Caspase-3 and PARP protein of U2-OS cells after treated with 20 μmol/L chloroquine and CCT128930 alone or combination for 24 h. RESULTS： Compared with blank control， the apoptotic rate of U2-OS cells increased after CCT128930 treatment （P＜0.01）， and the expression of Caspase-3， Caspase-8， Caspase-9 and PARP protein increased； the proportion of LC3-Ⅱ/LC3-Ⅰ increased （P＜0.05 or P＜0.01）； the expression of GFP-LC3 protein increased. CCT128930 combined with chloroquine reduced the viability of U2-OS cells， the protein expression of Caspase-3 and PARP. CONCLUSIONS： CCT128930 can induce the apoptosis and autophagy of U2-OS cells. Blocking autophagy can enhance the toxicity of CCT128930 to U2-OS cells.