Objective To study the effect of axitinib on the proliferation and apoptosis of human lung adenocarcinoma PC9 cells and its mechanism. Methods PC90 cells were treated with different concentrations (0, 0.125, 0.25, 0.5, 1, 2, 4, 8, 16, 32, and 64 μmol/L) of axitinib for 72 h, and half-inhibitory concentration (IC50) was calculated. The cell proliferation ability was detected by CCK-8 method. Plate cloning experiments were performed to observe the effect of axitinib on the formation of PC9 cell clones. The mitochondrial membrane potential and apoptosis of PC9 cells were detected by flow cytometry. The expression of cleaved-Caspase-3 protein in PC9 cells was detected by Western blot. Results Asitinib inhibited the proliferation of PC9 cells in a concentration-dependent manner. The IC50 at 72 h was 10.18μmol/L. The clone formation rates of PC9 cells were (100.0±3.2)％, (58.6±2.7)％, (29.3±3.3)％, and (10.9±3.0)％10 d after treatment with 0, 1, 2 and 4 μmol/L axitinib, and the difference was statistically significant (F= 316.922, P< 0.01). The apoptotic rate of PC9 cells at early and late stages increased after treatment with different concentrations of axitinib for 48 h, and the differences were statistically significant (both P< 0.01). After treatment with 0, 4, 8 and 16 μmol/L axitinib for 24 h, the percentage of PC9 cells with low mitochondrial membrane potential was (11.9±1.9)％, (38.5±2.3)％, (56.3±2.7)％, and (76.9±3.1)％, and the difference was statistically significant (F=234.320, P<0.01). The expression level of cleaved-Caspase-3 protein in PC9 cells increased, and the relative expression levels were 1.00±0.04, 1.26±0.09, 1.78±0.12, and 2.10±0.11, respectively, and the difference was statistically significant (F=55.670, P<0.01). Conclusions Axitinib could inhibit the proliferation of human lung adenocarcinoma PC9 cells. Axitinib induces the apoptosis of PC9 cells possibly through decreasing the mitochondrial membrane potential of PC9 cells.