The intrinsically dual nature of c-Myc function in growth and apoptosis and c-Myc-mediated apoptosis in normal cells requires wild-type p5334, however, the mechanisms of c-Myc-induciable apoptosis and how c-Myc and p53 involved in cancer cell apoptosis are not fully clarified. p53 is a well-known tumor suppressor protein, its overexpression can induce up-regulation of BAX and mitochondria-dependent apoptosis35. Our results were consistent with the references. Dehy, CD and VOSL treatment all can up-regulate the expression of p53, and increase the ratio of BAX to BCL-2. BAX and BCL-2 are both the BCL-2 family members, which serve as critical regulators of the mitochondrial-dependent apoptotic pathway. Thereinto, BCL-2 negatively regulates apoptosis and promotes cell survival, whereas BAX acts as a positive regulator of apoptosis to stimulate mitochondrial damage. The rise in ratio of BAX to BCL-2 will cause an opening of the mitochondrial permeability transition pore, which results in releasing pro-apoptotic proteins from the intermembrane space into the cytosol and triggering the mitochondrial-dependent apoptotic pathway3637. Moreover, phosphorylation of 14-3-3 was dramatically increased and phosphorylation of BID was decreased in the VOSL-treated group. Phosphorylation of 14-3-3 will induce dephosphorylation of BAD. Dephosphorylated BAD and dephosphorylated BID were translocated to mitochondria, where they associate with Bcl-2/Bcl-x(L) to induce the mitochondrial-dependent apoptosis38. Taken together, CD and VOSL treatment can up-regulate the expression of p53, down-regulate the phosphorylation levels of BID and BAD and increase the ratio of BAX to BCL-2, to trigger the mitochondrial-dependent apoptotic pathway.