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首页> 外文期刊>Radiation Research: Official Organ of the Radiation Research Society >Purvalanol A enhances cell killing by inhibiting up-regulation of CDC2 kinase activity in tumor cells irradiated with high doses of X rays
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Purvalanol A enhances cell killing by inhibiting up-regulation of CDC2 kinase activity in tumor cells irradiated with high doses of X rays

机译：普萘洛尔A通过抑制高剂量X射线照射的肿瘤细胞中CDC2激酶活性的上调来增强细胞杀伤力

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摘要

To clarify the relationship between CDC2 kinase activity and radiation-induced apoptosis, we examined whether the cyclin-dependent kinase (CDK) inhibitor purvalanol A enhanced radiation-induced apoptosis in gastric tumor cells. MKN45 cells exposed to 20 Gy of X rays increased the CDC2 kinase activity and the expression of regulatory proteins (phospho-CDC2 and cyclin B1) of the G(2)/M phase, followed by activation of the G(2)/M checkpoint, whereas the treatment of X-irradiated MKN45 cells with 20 mu M purvalanol A suppressed the increase in the CDC2 kinase activity and expression of the G(2)/M-phase regulatory proteins and reduced the fraction of the cells in the G,/M phase in the cell cycle. Furthermore, this treatment resulted in not only a significant increase in radiation-induced apoptosis but also the loss of clonogenicity in both MKN45 (p53-wild) and MKN28 (p53-mutated) cells. The expression of anti-apoptosis proteins, inhibitor of apoptosis protein (IAP) family members (survivin and XIAP) and BCL2 family members (Bcl-X-L and Bcl-2), in purvalanol A-treated cells with and without X rays was significantly lower than for cells exposed to X rays alone. These results suggest that the inhibition of radiation-induced CDC2 kinase activity by purvalanol A induces apoptosis through the enhancement of active fragments of caspase 3. (c) 2007 by Radiation Research Society.
机译：为了阐明CDC2激酶活性与辐射诱导的凋亡之间的关系，我们检查了细胞周期蛋白依赖性激酶（CDK）抑制剂嘌呤醇A是否增强了胃肿瘤细胞中辐射诱导的凋亡。暴露于20 Gy的X射线的MKN45细胞增加CDC2激酶活性和G（2）/ M期的调节蛋白（磷酸CDC2和细胞周期蛋白B1）的表达，然后激活G（2）/ M检查点，而X辐射的MKN45细胞用20μM的嘌呤醇A处理抑制了CDC2激酶活性的增加和G（2）/ M期调节蛋白的表达，并减少了G中细胞的比例，/细胞周期处于M期。此外，这种治疗不仅导致辐射诱导的细胞凋亡显着增加，而且导致MKN45（p53野生）和MKN28（p53突变）细胞的克隆形成性丧失。抗-凋亡蛋白，凋亡抑制蛋白（IAP）家族成员（survivin和XIAP）和BCL2家族成员（Bcl-XL和Bcl-2）在接受和不接受X射线的嘌呤醇A处理的细胞中的表达明显降低比单独暴露于X射线的细胞要强。这些结果表明，通过戊四醇A抑制辐射诱导的CDC2激酶活性通过增强胱天蛋白酶3的活性片段来诱导凋亡。

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