Kinetin riboside preferentially induces apoptosis by modulating Bcl-2 family proteins and caspase-3 in cancer cells

被引：63

作者：

Choi, Bo-Hwa ^{[1
]}

Kim, Wanil ^{[3
]}

Wang, Qiuxia Chelsia ^{[1
]}

Kim, Dong-Chan ^{[3
]}

Tan, Swee Ngin ^{[2
]}

Yong, Jean Wan Hing ^{[2
]}

Kim, Kyong-Tai ^{[3
]}

Yoon, Ho Sup ^{[1
]}

机构：

[1] Nanyang Technol Univ, Sch Biol Sci, Singapore 637511, Singapore

[2] Nanyang Technol Univ, Natl Inst Educ, Singapore, Singapore

[3] Pohang Univ Sci & Technol, Div Mol & Life Sci, Pohang, South Korea

来源：

CANCER LETTERS | 2008年 / 261卷 / 01期

关键词：

kinetin riboside; apoptosis; caspase-3; Bcl-2; cancer;

D O I：

10.1016/j.canlet.2007.11.014

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Here, we demonstrate that kinetin riboside (KR), a cytokinin analog, induces apoptosis in HeLa and mouse melanoma B16F-10 cells. KR disrupted the mitochondrial membrane potential and induced the release of cytochrome c and activation of caspase-3. Bad were upregulated while Bcl-2 was down-regulated under KR exposure. A tumor growth in mice was dramatically suppressed by KR. In contrast, human skin fibroblast CCL-116 and bovine primary fibroblast cells show resistances to KR and no significant changes in Bad, Bcl-X-L, and cleaved PARP were observed. Our data suggest that KR selectively induces apoptosis in cancer cells through the classical mitochondria dependent apoptosis pathway. (C) 2007 Elsevier Ireland Ltd. All rights reserved.

引用

页码：37 / 45

页数：9

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