cells. METHODS: The effects of apigenin on the growth, clone formation and proliferation of human gastric carcinoma SGC-7901 cells were observed by MTT, clone-forming assay, and morphological observation. Fluorescent staining and flow cytometry analysis were used to detect apoptosis of cells. RESULTS: Apigenin obviously inhibited the growth, clone formation and proliferation of SGC-7901 cells in a dosedependent manner. Inhibition of growth was observed on d 1 at the concentration of 80μmol/L, while after 4 d, the inhibition rate(IR)was 90%. The growth IRs at the concentration of 20, 40, and 80μmol/L were 38%, 71%, and 99% respectively on the 7th d. After the cells were treated with apigenin for 48h, the number of clone-forming in control, 20, 40, and 80μmol/L groups was 217±16.9, 170±11.1(P<0.05), 98±11.1(P<0.05), and 25±3. 5(P<0.05)respectively. Typical morphological changes of apoptosis was found by fluorescent staining. The cell nuclei had lost its smooth boundaries, chromatin was condensed, and cell nuclei were broken. Flow cytometry detected typical apoptosis peak. After the cells were treated with apigenin for 48h, the apoptosis rates were 5.76%, 19.17%, and 29.30% respectively in 20, 40, and 80μmol/L groups. CONCLUSION: Apigenin shows obvious inhibition on the growth and clone formation of SGC-7901 cells by inducing apoptosis.