Objective：This study aims to explore the inhibitory effect and mechanism of sulforaphane （SFN） on proliferation and migration of mouse lewis lung cancer cells （LLC）. Methods：CCK-8 method was used to identify the effect of SFN on LLC proliferation. Flow cytometry technology was used to detect the effect of SFN on cell cycle and apoptosis of LLC cells. DCFH-DA probe was used to detect the ROS expression in LLC cells. The effect of SFN on ERK signaling pathway in LLC cells was detected by Western blot. Finally，C56BL/6 mouse lung cancer tumor model was established by subcutaneous injection. After modeling，the experimental group and the control group were given SFN and PBS gavage treatment respectively，to detect the effect of SFN treatment on mouse tumors. Results：Cell experiments confirmed that SFN can significantly inhibit the proliferation and promote the apoptosis of LLC cells（P < 0.05）. With the increase of SFN concentration，the proportion of late apoptosis of LLC cells gradually increased（P < 0.05）. Cell cycle analysis showed that 12.5 μmol/L and 25.0 μmol/L SFN treatment reduced the proportion in G1 phase（P < 0.05）and increased the proportion of LLC cells in G2/M phase（P < 0.01）. The expression of cycle-related genes CyclinD1，CDK4，CDK6，CyclinB1 and CDK1 decreased significantly（P < 0.01）. Western blot suggested that SFN promoted ERK phosphorylation and increased Nrf2 expression in LLC cells（P < 0.05）. The flow test results showed that SFN could significantly increase ROS level in LLC cells. The results of animal experiments showed that the tumor volume of SFN treated mice was significantly smaller than that of control group（P < 0.05）. Conclusion：In vivo and in vitro experiments confirmed that SFN triggered ERK phosphorylation，which increased the expression of Nrf2，improved the expression level of ROS and blocked cell cycle，thus accelerating apoptosis and inhibiting the growth of tumor cells. SFN may be a safe and effective anti-cancer drug.