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首页> 外文期刊>International Journal of Radiation Biology: Covering the Physical, Chemical, Biological, and Medical Effects of Ionizing and Non-ionizing Radiations >Protein synthesis-dependent apoptotic signalling pathway in X-irradiated MOLT-4 human leukaemia cell line.
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Protein synthesis-dependent apoptotic signalling pathway in X-irradiated MOLT-4 human leukaemia cell line.

机译：X射线照射的MOLT-4人白血病细胞系中蛋白质合成依赖性凋亡信号通路。

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PURPOSE: To demonstrate whether protein synthesis is required for ionizing radiation-induced apoptosis through activation of caspases in human leukaemia cell line MOLT-4, the effects of a protein synthesis inhibitor, cycloheximide, on the apoptotic signalling pathway including the activation of caspase family and stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), and the expression of Fas/CD95/APO-1 (Fas) were examined in X-irradiated MOLT-4 cells. MATERIALS AND METHODS: MOLT-4 cells pretreated with 0.5 microg/ml cycloheximide for 1h were exposed to 7.5Gy of X-rays. The appearance of apoptosis, expression of Fas, activation of caspases-3, -8, -9, SAPK/JNK and AP-1, the release of mitochondrial cytochrome-C and the formation of death-induced signalling complex (DISC) between Fas and the Fas-associated death domain (FADD) were measured by fluorescence microscopy, Western blotting, flow cytometry, gel shift assay and immunoprecipitation, respectively. RESULTS: Nuclear fragmentation and chromatin condensation were observed at 6 h after X-irradiation and gradually increased up to 12 h. These phenomena were significantly attenuated by cycloheximide. Cycloheximide also inhibited the activation of caspases and AP-1, the expression of Fas, the formation of DISC and the release of cytochrome-C, but not the activation of SAPK/JNK in X-irradiated MOLT-4 cells. CONCLUSION: These results indicate that apoptosis of X-ray-induced MOLT-4 cells is dependent on the activation of caspases regulated by de novo protein synthesis through SAPK/JNK activation.
机译：目的：为了证明是否需要通过激活人类白血病细胞系MOLT-4中的半胱氨酸蛋白酶来电离辐射诱导的凋亡而进行蛋白质合成，蛋白质合成抑制剂环己酰亚胺对凋亡信号通路的影响，包括胱天蛋白酶家族的激活和在X射线照射的MOLT-4细胞中检测了应激活化蛋白激酶/ c-Jun N-末端激酶（SAPK / JNK）和Fas / CD95 / APO-1（Fas）的表达。材料与方法：将0.5μg/ ml环己酰亚胺预处理的MOLT-4细胞暴露于7.5Gy的X射线中。 Fas之间的凋亡，Fas表达，caspases-3，-8，-9，SAPK / JNK和AP-1的激活，线粒体细胞色素C的释放以及死亡诱导信号复合物（DISC）的形成Fas相关的死亡域（FADD）分别通过荧光显微镜，Western印迹，流式细胞术，凝胶位移测定和免疫沉淀法测定。结果：X射线照射后6 h观察到核碎裂和染色质浓缩，直至12 h逐渐增加。这些现象被环己酰亚胺显着减弱。环己二酰亚胺还抑制X射线照射的MOLT-4细胞中的半胱氨酸蛋白酶和AP-1的激活，Fas的表达，DISC的形成和细胞色素C的释放，但不抑制SAPK / JNK的激活。结论：这些结果表明，X射线诱导的MOLT-4细胞的凋亡依赖于从头蛋白合成通过SAPK / JNK激活调节的胱天蛋白酶的激活。

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