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激动素核糖苷通过调节癌细胞中的Bcl-2家族蛋白和半胱天冬酶-3优先诱导细胞凋亡。

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

作者信息

Choi Bo-Hwa, Kim Wanil, Wang Qiuxia Chelsia, Kim Dong-Chan, Tan Swee Ngin, Yong Jean Wan Hong, Kim Kyong-Tai, Yoon Ho Sup

机构信息

School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, Singapore 637511, Singapore.

出版信息

Cancer Lett. 2008 Mar 8;261(1):37-45. doi: 10.1016/j.canlet.2007.11.014. Epub 2007 Dec 26.

DOI:10.1016/j.canlet.2007.11.014
PMID:18162289
Abstract

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.

摘要

在此,我们证明了激动素核糖苷(KR),一种细胞分裂素类似物,可诱导人宫颈癌HeLa细胞和小鼠黑色素瘤B16F - 10细胞凋亡。KR破坏线粒体膜电位,诱导细胞色素c释放并激活caspase - 3。在KR作用下,促凋亡蛋白Bad上调而抗凋亡蛋白Bcl - 2下调。KR显著抑制了小鼠体内肿瘤的生长。相反,人皮肤成纤维细胞CCL - 116和牛原代成纤维细胞对KR具有抗性,且未观察到Bad、Bcl - X(L)和裂解的PARP有明显变化。我们的数据表明,KR通过经典的线粒体依赖性凋亡途径选择性地诱导癌细胞凋亡。

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Kinetin riboside preferentially induces apoptosis by modulating Bcl-2 family proteins and caspase-3 in cancer cells.激动素核糖苷通过调节癌细胞中的Bcl-2家族蛋白和半胱天冬酶-3优先诱导细胞凋亡。
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