Radiosensitization of oral cancer cells by expressing abnormalHuntingtin

本研究的目的是探讨肿瘤细胞应该通过表达异常的Hungtingtin蛋白来放射增敏的假设，因为据报道，在表达这种蛋白的神经元中，由于DSB修复所必需的Ku70耗尽，DNA双链断裂（DSB）的修复被抑制。我们发现，肿瘤细胞形成核包涵体表现出抑制DSB修复和放射增敏作用。作为放射增敏策略，必须获得有效的表达，并且需要进一步的研究。

The purpose of this study was to explore the hypothesis that tumor cells should be radiosensitized by expressing the abnormal Hungtingtin protein because the repair of DNA double strand breaks (DSB) is reported to be inhibited in neurons expressing such a protein due to exhaustion of Ku70 essential for the DSB repair. We found that tumor cells forming nuclear inclusion bodies exhibit inhibition of DSB repair and radiosensitization. Efficient expression must be obtained as a radiosensitizing strategy and further study is required.