端粒DNA双链断裂损伤修复依赖于同源重组和替代型非同源末端融合机制。同源重组机制不仅在端粒DNA双链断裂损伤修复中扮演重要角色，还在端粒酶阴性肿瘤细胞端粒长度维持中具有重要作用。目前，端粒DNA双链断裂损伤修复的蛋白调控机制并不清楚，端粒酶阴性肿瘤细胞端粒长度维持分子机制尚待解决。我们前期研究发现：1）在DNA双链断裂损伤情况下，染色体结构维持蛋白1（SMC1）发生磷酸化并结合到端粒DNA损伤位点；2）当SMC1被敲低表达时，端粒DNA双链断裂损伤信号显著增加；3）敲低SMC1蛋白表达水平显著增强端粒酶阴性肿瘤细胞中C-overhang和C-circles的量。结果表明SMC1在端粒DNA双链断裂损伤修复以及端粒酶阴性肿瘤细胞中具有重要作用，但其作用机制有待进一步研究。该研究不仅拓展了端粒DNA损伤研究领域，同时还为端粒酶阴性肿瘤治疗提供新思路。

Double-strand break repair of telomeric DNA depends on homologous recombination and alternative non-homologous end joining. Homologous recombination plays an important role in telomeric DNA double-strand break repair, and it's also important for telomerase-negative tumor cells to maintain telomere length. The regulation of telomeric DNA double-strand break repair remains poorly understood, and the molecular mechanism underlying telomere maintenance in telomerase-negative tumor cells needs to be solved. In previous study, we found that phosphorylated SMC1 can bind to damaged telomeric DNA, and that SMC1 knockdown increase telomere DNA damage response. we also found that SMC1 knockdown elevate the level of C-overhang and C-circles in telomerase-negative tumor cells. These results suggest that SMC1 plays an important function both in telomeric DNA double-strand break repair and in telomerase-negative tumor cells, but further study is required to discover the underlying mechanism. This study promote the theoretical research in telomeric DNA damage and provide an important implication for the therapy of telomerase-negative tumors.