〔Abstract〕 Objective To research the effects of sodium valproate(VPA) on proliferation, migration of human lung adenocarcinoma PC9 cells in different concentrations and its possible mechanism. Methods PC9 cells were divided into control group(0 mmol/L VPA)and experimental groups(2, 4, 8 and 16 mmol/L VPA), and they were cultured in vitro. CCk-8 and scratch test were used to detect the effects of VPA of different concentrations on the proliferation and migration ability of PC9 cells under different time conditions. The effects of VPA on lactate dehydrogenase activity and lactic acid production in different concentrations were detected by lactate dehydrogenase activity assay kit and lactate quantitative assay kit respectively. ELISA was used to detect the expression levels of E-caducin( E-cad) and vimentin( VIM) in cell culture supernatant and in cells. Results CCK-8 result revealed that VPA had a concentration-dependent and time-dependent cell proliferation inhibition effect on PC9 cells(P<0.05). The scratch test result indicated that the migration distances of the experimental groups were smaller than that of the control group(P<0.05),and the migration distance gradually decreased when VPA concentration increased(P<0. 05). LDH activity and LD test results indicated that the activity of LDH and LD production of the experimental groups were significantly lower than that of the control group(P<0.05). LDH activity and LD production gradually decreased when VPA concentration increased(P<0.05). ELISA results indicated that the cell culture supernatant and cells in the experimental groups had more E-cad protein than the control group,and the concentration of E-cad increased gradually when VPA concentration increased(P<0. 05). The cell culture supernatant and cells in the experimental group had less VIM protein than the control group,and VIM protein concentration gradually decreased when VPA concentration increased(P<0.05). Conclusion The proliferation and migration of PC9 cells in vitro can be restrained by VPA,possibly by restraining aerobic glycolysis and epithelial mesenchymal transformation.