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Cellular, Molecular, and Tumor Biology 81: Apoptosis-inducing Agents

Abstract #4121

Mechanisms of proapoptotic properties of curcumin in chronic and acute myeloid leukemia

Hanyang University, Seoul, Republic of Korea, Department of Internal Medicine, Seoul National University, College of Medicine, Cancer Research Center, Seoul, Republic of Korea, Cancer Research Center, Seoul National University, Seoul, Republic of Korea, Samsung Biomedical Research Center, Seoul, Republic of Korea

Curcumin, a yellow coloring agent from turmeric (Curcuma longa Linn, Zingiberaceae), possesses strong antimutagenic and anticarcinogenic activities. However, molecular mechanisms underlying its anticancer activities remain to be defined in both chronic (CML) and acute myeloid leukemia (AML). To investigate whether curcumin induces apoptosis, pAkt, Bcl-2 family, Caspase 3 and cell cycle proteins including p53, Erk, P21, cyclin D and pRb were examined for their expression by western analysis. CML cell line (K562) and AML cell line (CCRF-SM) were treated with 50µM curcumin. Curcumin caused dose-dependent apoptosis in both CML and AML cells. Apoptosis was preceded by the sequential dephosphorylation of Akt, down-regulation of the anti-apoptotic Bcl-2 and activation of caspase 3. When the cells were pre-treated with cyclosporin A, dephosphorylation of Akt markedly decreased and cell viability increased. These indicated that curcumin induced apoptosis by inactivation the Akt-related cell survival pathway, providing a new mechanism for curcumin-induced cytotoxicity. Also, the expression of P21 and p53 were elevated and that of cyclin D decreased with curcumin treatment. Our study indicated that curcumin could induce apoptosis by disturbing cell cycle progression in both chronic and acute myeloid leukemia.