非同源末端连接是哺乳动物最主要的DNA双链断裂(DSB)连接方式。肿瘤细胞非同源末端连接能力的提高与其放化疗抵抗有关,抑制肿瘤细胞非同源末端连接能力,可能增加其对放化疗的敏感性。因此,参与非同源末端连接的修复因子可能成为肿瘤分子靶向治疗及放化疗增敏的新治疗点。
Non- homologous end joining (NHEJ) is the major pathway for repairing DNA double- strand break (DSB) in mammalian species. The capacity of NHEJ increases in tumor cell ,which plays a role in radiation/chemotherapy-resistant agent. Inhibiting DSB rejoining may play a crucial role in the enhancement of Cellular radiation/chemotherapy-sensitizing. Thus, the protein molecule enrolled in NHEJ may be new potential targets for radiation/chemotherapy-sensitizing.