Radiosensitization of oral cancer cells by expressing abnormalHuntingtin

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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.