Radiation-induced apoptosis of tumor cells is facilitated by inhibition of the interaction between Survivin and Smac/DIABLO
Radiation-induced apoptosis of tumor cells is facilitated by inhibition of the interaction between Survivin and Smac/DIABLO
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DOI：
10.1016/j.canlet.2007.09.017
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发表时间：
2008-01-18
期刊：
影响因子：
9.7
通讯作者：
Inanami, Osamu
中科院分区：
文献类型：
--
作者：
Ogura, Aki;Watanabe, Yasuko;Inanami, Osamu
为了探讨实体瘤细胞辐射抗性的机制，我们构建了两个Survivin突变体T34 A和D53 A的表达载体。当T34 A和D53 A在NIH 3 T3、A549和HeLa细胞中过表达时，辐射诱导的凋亡显著增强。此外，我们研究了Survivin与Smac/DIABLO在过表达这些突变体的细胞中的结合能力。免疫共沉淀分析显示突变形式的Survivin、D53 A和T34 A可以与Smac/DIABLO结合，但与真实形式相比亲和力低得多。这些结果表明，通过T34 A和D53 A的过表达抑制Survivin和Smac/DIABLO之间的相互作用，增加了辐射诱导的肿瘤细胞凋亡。(c)2007爱思唯尔爱尔兰有限公司保留所有权利。
To investigate the mechanism of radioresistance of solid tumor cells, we created two expression vectors encoding Survivin mutants, T34A and D53A. When T34A and D53A were overexpressed in NIH3T3, A549 and HeLa cells, radiation-induced apoptosis was significantly enhanced. Furthermore, we examined the binding capability of Survivin with Smac/DIABLO in the cells that overexpressed these mutants. Coimmunoprecipitation analysis revealed that mutant form of Survivin, D53A and T34A could bind to Smac/DIABLO, but with much less affinity compared to the authentic form. These results suggest that radiation-induced apoptosis of tumor cells is increased by inhibition of the interaction between Survivin and Smac/DIABLO through overexpression of T34A and D53A. (c) 2007 Elsevier Ireland Ltd. All rights reserved.