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Ju, J., Hong, J., Zhou, J.N., Pan, Z., Bose, M., Liao, J., Yang, G.Y., Liu, Y.Y., Hou, Z., Lin, Y., Ma, J., Shih, W.J., Carothers, A.M. and Yang, C.S. (2005) Inhibition of intestinal tumorigenesis in Apcmin/+ mice by (-)-epigallocatechin-3-gallate, the major catechin in green tea. Cancer Research, 65, 10623-10631. doi:10.1158/0008-5472.CAN-05-1949

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• TITLE: Cancer chemoprevention through the induction of apoptosis by natural compounds

  AUTHORS: Toshiya Kuno, Testuya Tsukamoto, Akira Hara, Takuji Tanaka

  KEYWORDS: Cancer Chemoprevention; Apoptosis; Natural Compounds

  JOURNAL NAME: Journal of Biophysical Chemistry, Vol.3 No.2, May 29, 2012

  ABSTRACT: As cell and tissue homeostasis are mediated by the balance between proliferation and apoptosis, controlling this balance is important for cancer chemoprevention. Cancer chemoprevention can be achieved by the use of natural, synthetic or biologic compounds that reverse, suppress or prevent the development of epithelial malignancies. Natural compounds including flavonoids are able to reduce oxidative stress, which is the most likely mechanism mediating the protective effects against cancer development. In addition, in vitro and in vivo studies have suggested that flavonoids, such as (-)-epigallocatechin-3-gallete (EGCG), quercetin, and curcumin, act by induction of apoptosis. Several natural compounds inhibit cell proliferation and angiogenesis. Certain natural products have been shown to inhibit the activation of nuclear factor kappa B (NF-κB) and Akt signaling pathways, both of which are known to maintain a homeostatic balance between cell survival and apoptosis. Understanding the mechanism of these natural products will contribute to the development of more specific preventive strategies against cancer development. Here we focus on the ability of natural cancer chemopreventive agents to induce apoptosis, and attempt to provide evidence for the preventive and therapeutic effects of natural compounds, EGCG, quercetin, and curcumin, in a succinct manner highlightingκand Akt signaling pathways in vivo.