Tannic acid-induced apoptosis and -enhanced sensitivity to arsenic trioxide in human leukemia HL-60 cells

Tannic acid (TA), a glucoside of gallic acid polymer, has been shown to possess anti-bacterial, anti-enzymatic, anti-tumor and astringent properties. However, the anti-cancer activity of TA in leukemia is still obscure. In this Study, we showed TA-induced apoptotic death in acute myeloid leukemia (AML) HL-60 cells via dose- and time-dependent manner as well as increase of sub-G1 fraction. chromosome condensation. and DNA fragmentation. Further analysis demonstrated the involvement of activation of caspase cascade. cleavage of poly (ADP-ribose) polymerase (PARP), disruption of mitochondrial membrane potential, and release of Cytochrome C, in TA-induced apoptosis. These effects were probably associated with the increase of intracellular Superoxide in mitochondrial signaling pathway which attributed 10 the down-regulation of superoxide dismutase (SOD). Notably, a low dose of TA is sufficient to aggravate arsenic trioxide (As2O3)-induced cytotoxicity in HL-60 cells. Altogether, this Study suggested the effects of TA to induce apoptosis in HL-60 and therapeutic potential in AML being an adjunct to As2O3. (C) 2008 Elsevier Ltd. All rights reserved.