To confirm the results, 740Y-P (a PI3K agonist, Selleck, USA, S7865) and LY294002 (a PI3K inhibitor, Selleck, USA, S1105) were used to treat MNNG cells alone or combined with C 18 H 17 NO 6 for 48 h. Firstly, we found that 740Y-P at 20 µM remarkably increased the proliferation ( Figure 3A     C 18 H 17 NO 6 group (p<0.05). After co-incubation with 740Y-P, these changes were marked rescued (p<0.05). Secondly, the protein expression levels of MMP-2, MMP-9, E-cadherin, N-cadherin, and Vimentin were evaluated. As shown in Figures  3G and 3H, the protein expression levels of MMP-2, MMP-9, N-cadherin, and Vimentin were significantly downregulated following treatment with 4 µM C 18 H 17 NO 6 (p<0.05). 740Y-P at 20 µM remarkably rescued this decrease (p<0.05). We obtained the opposite results in the protein expression levels of E-cadherin. Finally, to investigate whether the PI3K/AKT pathway participates in the inhibitory effect of C 18 H 17 NO 6 on MNNG cells, the cells were incubated with 740Y-P (20 µM), LY294002 (20 µM) alone, or in combination with C 18 H 17 NO 6 (4 µM) for 48 h. Compared to the control group, 740Y-P at 20 µM remarkably upregulated the protein expression of p-PI3K and p-AKT (p<0.05), and C 18 H 17 NO 6 at 4 µM and LY294002 at 20 µM treatment resulted in remarkably downregulated the protein expression of p-PI3K and p-AKT (p<0.05). After co-incubation with 740Y-P, C 18 H 17 NO 6 -dependent inhibition of the PI3K/AKT signaling pathway was eliminated. Co-incubation with LY294002 enhanced suppression of the PI3K/AKT signaling pathway (Figures 3I, 3J). These **data** at least partially suggest that C 18 H 17 NO 6 weakens MNNG cell proliferation, migration, and invasion by inhibiting the PI3K/AKT signaling pathway.