PARP抑制剂作为靶向DNA损伤修复抑制剂，近年来在肿瘤治疗的相关研究中取得重要进展，但在乳腺癌细胞放射敏感性中的相关研究甚少。基于ER、PR、HER-2的乳腺癌分子分型作为重要的预后和预测指标已被广泛应用于指导临床治疗，我们前期的研究结果提示不同分子亚型的乳腺癌细胞对PJ34（第三代PARP抑制剂）的敏感性有所不同，存在差异的可能原因为DNA损伤修复能力不同，在此基础上，我们提出假设：PARP抑制剂可能通过对放射线所致DNA损伤修复不同程度的抑制，对不同分子分型的乳腺癌细胞有不同的放射增敏作用。我们根据ERa和HER-2这两个关键的分型指标表达的不同，建立了模拟临床上四种不同分子亚型的乳腺癌细胞模型，拟采用细胞克隆形成实验、免疫荧光、流式细胞术、western blot等手段，从分子、细胞和体内动物整体水平研究PJ34对不同分子分型乳腺癌细胞的放射增敏效应及其中可能的机制。

We aim to investigate the impact of poly ADP-ribose polymerase inhibitor (PARPi) on the different molecular types of breast cancer cell. It has been well addressed that the PARPi work as an important targeted inhibitor for DNA damage, especially in glioblastoma, lung cancer and rectal cancer. But the report is relatively rare in breast cancer. Recently the molecular subtypes of breast cancer based on ER, PR and Her-2 have been extensively applied in the diagnosis and treatment of breast cancer, guiding the principle of therapeutic decisions. The pilot result from our group has shown that the radiosensitivity is fairly different in various molecular subtypes of breast cancer when treated by the third generation of PARPi - PJ34, and we hypothesis that the difference on the radiosensitivity may be derived from the various ability of DAN damage repair in different breast cancer cell. We herein set up cell lines which mimic the molecular subtypes of breast cancer and plan to assess the effect of radiosentivity to the breast cancer cell of the PJ34 and investigate the potential mechanism by the cell clone forming study, immunofluorescence and westen blot.