To explore the potential effect and mechanism of Schisantherin A(SA) on the growth and metastasis of lung cancer cells.Methods:In this study，the non-small cell lung cancer cell lines A549 and H1299 were used as experimental objects.SA was dissolved in dimethyl sulfoxide(DMSO)，and A549 and H1299 was incubated with different concentrations of SA(0 μM，5 μM，10 μM，20 μM，50 μM) for 24 h，48 h and 72 h.Then，Cell Counting Kit-8(CCK-8) was used to detect cell proliferation，FC500 flow cytometer was used to analyze cell apoptosis，wound healing experiment was used to evaluate cell migration，and Transwell was used to detect cell invasion.Real-time quantitative reverse transcription polymerase chain reaction(qRT-PCR) was used to detect CCAT1mRNA levels in cells.Western blot was used to detect the protein expression levels of p-PI3K，PI3K，p-AKT，AKT，PTEN，E-cadherin，MMP2 and MMP9 in cells.Results:Compared with untreated cells，SA reduced the cell viability of A549 and H1299 in a concentration and time-dependent manner(P<0.05).Compared with the DMSO group，the apoptosis rate of A549 and H1299 cells in the SA 10 μM group was significantly increased by 5.71 times and 3.48 times(P<0.001)，the wound healing area of A549 and H1299 cells in the SA 10 μM group was significantly reduced by 63.42% and 59.15%(P<0.001)，and the number of invasion cells of A549 and H1299 cells in the SA 10 μM group was significantly reduced by 53.98% and 53.36%(P<0.001).Compared with the DMSO group，the protein expression levels of E-cadherin in A549 and H1299 cells in the SA 10 μM group increased，while the protein expression levels of MMP-2 and MMP-9 decreased(P<0.01); the mRNA and protein expression levels of CCAT1 in A549 and H1299 cells in the SA 10 μM group were lower(P<0.01); the protein expression of p-PI3K and p-AKT in A549 and H1299 cells in SA 10 μM group decreased significantly(P<0.01)，PTEN protein expression level increased significantly(P<0.01)，while PI3K and AKT protein expression levels did not change significantly(P>0.05).Conclusion:SA inhibits the growth and metastasis of lung cancer cells by inhibiting the CCAT1 and PI3K/AKT signaling pathways.