Induction of apoptosis by furanodiene in HL60 leukemia cells through activation of TNFR1 signaling pathway

被引：63

作者：

Ma, Enlong ^{[1
,2
]}

Wang, Xiaolong ^{[2
]}

Li, Yanchun ^{[2
]}

Sun, Xiuyan ^{[3
]}

Tai, Wenjiao ^{[2
]}

Li, Te ^{[2
]}

Guo, Tao ^{[1
]}

机构：

[1] Gen Hosp Shenyang Mil Reg, Dept Pharm, Shenyang 110016, Peoples R China

[2] Shenyang Pharmaceut Univ, Dept Pharmacol, Shenyang 110016, Peoples R China

[3] Univ Yantai, Sch Pharm, Yantai 264005, Peoples R China

来源：

CANCER LETTERS | 2008年 / 271卷 / 01期

关键词：

Furanodiene; Apoptosis; Leukemia; TNFR1;

D O I：

10.1016/j.canlet.2008.06.008

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Furanodiene, a natural product isolated from Curcuma wenyujin, has been reported to produce cytotoxic effect. In this study, we investigated its effects on human leukemia HL60 cells. Furanodiene induced apoptosis of HL60 cells, characterized by DNA fragmentation, cleavage of poly (ADP-ribose) polymerase (PARP), caspase-3, caspase-8 and caspase-9. In the Bcl-2 family proteins, Bid protein (a substrate of caspase-8) was activated by furanodiene, but Bcl-2, Bax and Bcl-xI proteins were not influenced by furanodiene stimulation. Moreover, furanodiene treatment caused the upregulation of tumor necrosis factor receptor I (TNFR1), the formation of TNFR1 complex and an obvious production of TNF-alpha in HL60 cells. The soluble TNFR I receptor effectively inhibited furanodiene-induced apoptosis. Taken together, furanodiene could inhibit the growth of leukemia cells via induction of apoptosis, and TNFR I-mediated extrinsic apoptotic pathway explains furanodiene-induced apoptosis. (C) 2008 Published by Elsevier Ireland Ltd.

引用

页码：158 / 166

页数：9

共 32 条

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