Objective: To investigate the effect of tanshinone IIA on gastric cancer SGC7901 cells in vitro and its influence on the NF-κB signaling pathway. Methods: SGC7901 cells were exposed to different concentrations (0.5, 1, 2 and 4 μg/mL) of tanshinone IIA for different lengths of time (24, 48 and 72 h), and then the cell proliferation was determined by MTT assay. In SGC7901 cells after exposure to tanshinone IIA (2 μg/mL) for 48 h, the apoptosis rate was measured by flow cytometry; the protein expressions of p65 subunit, IκB-α, phosphorylated IκB-α, IKK-α/β, and phosphorylated IKK-α/β were detected by Western blot; the DNA binding activity of NF-κB p65 subunit was detected by ELISA assay. Results: Results of MTT assay showed that tanshinone IIA (1, 2, and 4 μg/mL) significantly inhibited the proliferation of SGC7901 cells in a time- and concentration-dependent manner (all P<0.05). Apoptosis analysis showed that the apoptosis rate in tanshinone IIA treated cells was significantly higher than that in the control cells (P<0.05); measurement of the NF-κB signaling pathway showed that in tanshinone IIA treated cells compared with the control cells, the expression levels of p65 subunit, and IKK-β along with its phosphorylated form were significantly decreased (all P<0.05), and IκB-α expression level had no significant change (P>0.05) but its phosphorylated form was significantly reduced (P<0.05), while the levels of IKK-α and its phosphorylated form had no significant change (both P>0.05); the DNA binding activity of p65 subunit was significantly decreased (P<0.05). Conclusion: Tanshinone IIA can inhibit proliferation and induce apoptosis in gastric cancer SGC7901 cells, and the mechanism may probably be related with its suppresson of the activity of NF-кB signaling pathway.