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

doi:10.1016/j.leukres.2008.08.006

中山醫學大學機構典藏 CSMUIR > 醫學院 > 生化微生物免疫研究所 > 期刊論文 > Item 310902500/11467

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/11467

Title:	Tannic acid-induced apoptosis and -enhanced sensitivity to arsenic trioxide in human leukemia HL-60 cells.
Authors:	Chen, KS Hsiao, YC Kuo, DY Chou, MC Chu, SC Hsieh, YS Lin, TH
Contributors:	中山醫學大學
Keywords:	Tannic acid;Acute myeloid leukemia cells;Apoptosis;Superoxide;SOD
Date:	2009
Issue Date:	2015-07-21T08:15:46Z (UTC)
ISSN:	0145-2126
Abstract:	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).
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/11467 http://dx.doi.org/10.1016/j.leukres.2008.08.006
Relation:	Leuk Res. 2009 Feb;33(2):297-307.
Appears in Collections:	[生化微生物免疫研究所] 期刊論文

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