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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 >Decreased c-Myc expression and its involvement in X-ray-induced apoptotic cell death of human T-cell leukaemia cell line MOLT-4.
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Decreased c-Myc expression and its involvement in X-ray-induced apoptotic cell death of human T-cell leukaemia cell line MOLT-4.

机译：c-Myc表达降低及其参与人T细胞白血病细胞系MOLT-4的X射线诱导的凋亡细胞死亡。

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摘要

Purpose: To investigate the possible involvement of c-Myc and ceramide-c-Jun N-terminal kinase (JNK) pathway in X-ray-induced apoptotic cell death of MOLT-4 cells. Materials and methods: The expressions of c-Myc protein and c-myc mRNA after X-irradiation were analysed by Western blotting and RT-PCR between radiosensitive MOLT-4 and radioresistant variant Rh-1a cells with less JNK activation than the parental cells. Apoptotic cell death was determined by a dye exclusion test, the appearance of chromatin condensation and DNA fragmentation. The effect of a JNK activator anisomycin or c-Myc inhibitor peptides (Int-H1-S6A, F8A) on the amount of c-Myc protein and on the induction of apoptosis was investigated, respectively. Results: In X-irradiated MOLT-4 cells, amounts of both c-myc mRNA and c-Myc protein rapidly decreased, which was followed by apoptotic cell death, while little change or limited reduction of c-Myc protein was observed in X-irradiated Rh-1a cells with accompanying higher cell viability. Exposure of MOLT-4 and Rh-1a cells to c-Myc inhibitor peptides similarly induced apoptotic cell death with decreases of c-Myc protein. Anisomycin rapidly induced JNK activation and a subsequent decrease of c-Myc protein, causing cell death in MOLT-4 cells. On the other hand, Rh-1a cells were more resistant to anisomycin than parental MOLT-4 cells, showing less JNK activation and a delayed decrease of c-Myc protein. Conclusion: A decrease of c-Myc protein was considered important in X-ray-induced apoptotic cell death of MOLT-4 cells; activation of the JNK pathway caused reduction in the amounts of c-myc mRNA and c-Myc protein, and finally induced apoptotic cell death.
机译：目的：研究c-Myc和神经酰胺-c-Jun N末端激酶（JNK）途径在X射线诱导的MOLT-4细胞凋亡中的作用。材料与方法：通过Western blotting和RT-PCR分析放射线敏感性MOLT-4和抗辐射变异Rh-1a细胞之间的X-射线照射后c-Myc蛋白和c-myc mRNA的表达，JNK活化程度低于亲代细胞。通过染料排斥试验，染色质凝集和DNA片段化来确定凋亡细胞的死亡。分别研究了JNK激活茴香霉素或c-Myc抑制剂肽（Int-H1-S6A，F8A）对c-Myc蛋白含量和对细胞凋亡的诱导作用。结果：在X射线照射的MOLT-4细胞中，c-myc mRNA和c-Myc蛋白的量迅速减少，随后凋亡的细胞死亡，而在X-射线中观察到的c-Myc蛋白变化很小或有限地减少。辐射的Rh-1a细胞具有更高的细胞活力。 MOLT-4和Rh-1a细胞暴露于c-Myc抑制剂肽同样诱导凋亡细胞死亡，而c-Myc蛋白减少。 Anisomycin迅速诱导JNK活化并随后降低c-Myc蛋白，从而导致MOLT-4细胞死亡。另一方面，Rh-1a细胞比亲代MOLT-4细胞对茴香霉素的抗性更高，显示出更少的JNK活化和c-Myc蛋白的延迟减少。结论：c-Myc蛋白的减少被认为在X射线诱导的MOLT-4细胞凋亡中起重要作用。 JNK途径的激活导致c-myc mRNA和c-Myc蛋白数量的减少，并最终导致凋亡性细胞死亡。

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