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首页> 外文期刊>Journal of Radiation Research: Official Organ of the Japan Radiation Research Society >Inhibition of potential lethal damage repair and related gene expression after carbon-ion beam irradiation to human lung cancer grown in nude mice
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Inhibition of potential lethal damage repair and related gene expression after carbon-ion beam irradiation to human lung cancer grown in nude mice

机译：碳离子束辐照对裸鼠中生长的人肺癌的潜在致死性损伤修复及相关基因表达的抑制

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摘要

Using cultured and nude mouse tumor cells (IA) derived from a human lung cancer, we previously demonstrated their radio sensitivity by focusing attention on the dynamics of tumor clonogens and the early and rapid survival recovery (potential lethal damage repair: PLD repair) occurring after X-ray irradiation. To the authors' knowledge, this is the first study demonstrating gene expression in association with PLD repair after carbon-ion beam or X-ray irradiation to cancer cells. In this study we tried to detect the mechanism of DNA damage and repair of the clonogens after X-ray or carbon-ion beam irradiation. At first, colony assay method was performed after irradiation of 12 Gy of X-ray or 5 Gy of carbon-ion beam to compare the time dependent cell survival of the IA cells after each irradiation pass. Second, to search the genes causing PLD repair after irradiation of X-ray or carbon-ion beam, we evaluated gene expressions by using semi-quantitative RT-PCR with the selected 34 genes reportedly related to DNA repair. The intervals from the irradiation were 0, 6, 12 and 24 hr for colony assay method, and 0, 3, 18 hr for RT-PCR method. From the result of survival assays, significant PLD repair was not observed in carbon-ion beam as compared to X-ray irradiation. The results of RT-PCR were as follows. The gene showing significantly higher expressions after X-ray irradiation than after carbon-ion beam irradiation was PCNA. The genes showing significantly lower expressions after X-ray irradiation rather than after carbon-ion beam irradiation were RAD50, BRCA1, MRE11A, XRCC3, CHEK1, MLH1, CCNB1, CCNB2 and LIG4. We conclude that PCNA could be a likely candidate gene for PLD repair.
机译：我们使用源自人类肺癌的培养的裸鼠肿瘤细胞（IA），通过集中关注肿瘤克隆原的动力学以及术后发生的早期和快速生存恢复（潜在的致死性损伤修复：PLD修复）来证明其放射敏感性。 X射线照射。据作者所知，这是第一个证明基因表达与碳离子束或X射线照射癌细胞后与PLD修复相关的研究。在这项研究中，我们试图检测X射线或碳离子束照射后DNA损伤和克隆蛋白修复的机制。首先，在照射12 Gy的X射线或5 Gy的碳离子束之后进行菌落测定法，以比较每次照射后IA细胞的时间依赖性细胞存活率。其次，为了搜索在X射线或碳离子束照射后导致PLD修复的基因，我们使用半定量RT-PCR与报道的与DNA修复相关的34个基因进行了评估，评估了基因表达。对于菌落测定法，照射间隔为0、6、12和24小时，对于RT-PCR方法，为0、3、18小时。从生存分析的结果来看，与X射线辐照相比，在碳离子束中未观察到明显的PLD修复。 RT-PCR的结果如下。 X射线照射后的表达明显高于碳离子束照射后的表达的基因是PCNA。 X射线照射后而不是碳离子束照射后，表达明显降低的基因是RAD50，BRCA1，MRE11A，XRCC3，CHEK1，MLH1，CCNB1，CCNB2和LIG4。我们得出的结论是PCNA可能是PLD修复的可能候选基因。

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