Numerous studies showed that activation of AKT is positively correlated with cancer development, and c-Jun NH2-terminal kinase (JNK) can antagonize AKT-mediated survival signals by phosphorylating 14-3-3. In this study, the phosphorylation level of AKT was down-regulated (Fig. 4I and J) and the phosphorylation level of 14-3-3 was up-regulated (Fig. 4K and L) dose-dependently, with no obvious changes of the total AKT and 14-3-3 levels in the four test groups compared with the control group, and the ratios of p-AKT/AKT in the CD and VOSL treated groups were obviously lower than that in the Cos and Dehy treated groups, and the ratios of p-14-3-3/14-3-3 in the CD and VOSL treated groups were obviously higher than that in the Cos and Dehy treated groups.