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The development of advanced cervical cancer therapies is a particularly urgent need due to the strong side effects and toxicities of current treatments. Caffeic acid phenethyl ester (CAPE) exhibits broad-spectrum antitumor activities and little toxicity or side effects. In our previous study, caffeic acid para-nitro phenethyl ester (CAPE- p NO 2 ) significantly improved the effect of anti-platelet aggregation and attenuated myocardial ischemia. Based on this finding, we aimed to further explore the antitumor activity of CAPE- p NO 2 in cervical cancer cells and tumor xenografts. In addition, we assessed the biotransformation of CAPE- p NO 2 in cervical cancer cells. Our study demonstrated that both CAPE and CAPE- p NO 2 can inhibit cell proliferation via the induction of G2/M cell cycle arrest. More importantly, CAPE- p NO 2 dramatically induced cell apoptosis via significant down-regulation of pro-caspase-3, pro-caspase-9, Bcl-2, Cyclin B1 and Cdc2 and up-regulation of cleaved-caspase-3, Bax, CytoC and P21 Cip1 . Moreover, CAPE and CAPE- p NO 2 significantly suppressed the growth and angiogenesis of nude mice xenografts. CAPE and CAPE- p NO 2 were found to degrade into four and six metabolites, respectively. The metabolites of CAPE and CAPE- p NO 2 were different, and the major metabolic pathway may be phase II reactions. These results suggest that CAPE- p NO 2 induced cell apoptosis and cell cycle arrest via a strong regulatory effect on relevant apoptotic proteins. Therefore, CAPE- p NO 2 should be further studied as a potent anti-cancer agent.

Inhibited effects of CAPE-pNO2 on cervical carcinoma in vivo and in vitro and its detected metabolites