Much evidence showed that c-Myc plays a critical role in the control of cell proliferation, regulation of cell cycle, and serves as a link between proliferation and cell death by inducing p53-dependent apoptosis2021. c-Myc has been documented to be both a positive and a negative signal for induction of apoptosis22. It is well known that overexpression of c-Myc induces normal cell apoptosis23. However, down-regulation of c-Myc expression may be mandatory for induction of apoptosis in many cancer cells, such as leukemia cells24, prostate cancer cells25, lung cancer cells26, and liver cancer cells27. c-Myc is frequently overexpressed in cancer cells28, enhanced expression of c-Myc will lead to activation of Cdk/Rb/E2F pathway, which is critical for cell cycle progression from G1 into S phase20. Moreover, c-Myc plays an important role in controlling various genes endcoding protein-synthesis components and regulating the expression of critical proteins in DNA replication machinery2930. Therefore, its overexpression can activate the general apparatus for cellular metabolism and promote the process of DNA replication, so as to prepare cancer cell for continued proliferation. Conversely, deregulated c-Myc expression results in S phase arrest and cell apoptosis20. In addition, down-regulation of c-Myc expression can significantly decrease telomerase activity and inhibit growth of cancer cells3132. Therefore, reduction of c-Myc expression has been considered as a potential therapeutic strategy for cancer33. In the present study, Cos, Dehy, CD and VOSL treatment all can reduce the expression of c-Myc, inhibit MCF-7 cell proliferation and induce its apoptosis.