Abstract Title:

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

Abstract Source:

Leuk Res. 2008 Sep 12. PMID: 18790533

Abstract Author(s):

Kuo-Shuen Chen, Yung-Chin Hsiao, Dong-Yih Kuo, Ming-Chih Chou, Shu-Chen Chu, Yih-Shou Hsieh, Tseng-Hsi Lin


Full Citation: "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 to the down-regulation of superoxide dismutase (SOD). Notably, a low dose of TA is sufficient to aggravate arsenic trioxide (As(2)O(3))-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 by being an adjunct to As(2)O(3)."

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