PARP抑制剂的出现为BRCA1/2突变及铂治疗敏感的上皮性高级别浆液性卵巢癌HGSOC带来福音。但仍不能解释部分非BRCA突变患者治疗有效，或初始治疗敏感后对PRAP抑制剂耐药现象。前期申请人发现HR通路重要基因RAD51参与了HGSOC的耐药。由此我们设想转移细胞来源的外泌体中的miR-215-5p通过靶向作用RADX，抑制RADX的表达，进而促进PARP抑制剂Olaparib的耐药。我们利用高通量测序证实miR-215-5p可以通过外泌体从转移的卵巢癌细胞中传递到原位卵巢癌细胞中，结合体内，体外细胞生物学技术证明外泌体中的miR-215-5p通过靶向作用于RADX，最后利用Co-IP质谱技术证实RADX被招募到DNA的复制叉中，通过抑制RAD51来防止复制叉的崩解。研究揭示RADX的缺失可以部分恢复BRCA沉默的细胞对于PARP抑制剂的耐药，为临床PRAP抑制剂靶向治疗提供实验依据。

PARP inhibitors emerged as a new therapeutic approach for epithelial high grade serous ovarian cancer (HGSOC) patients, especially for those who are sensitive to platinum-based chemotherapy or with BRCA1/2 mutations in their genes. Yet this couldn’t account for the phenomena that a portion of non-BRCA patients gain benefits or convert into PARP inhibitor-resistant after being proved effective at the beginning. Previous applicants have found that RAD51, a crucial gene in the HR pathway, plays a part in drug-resistance of HGSOC. Thus we infer that miR-215-5p in exosomes derived from metastatic cells suppresses RADX expression specifically, therefore promoting drug-resistance of Olaparib---the PARP inhibitor. We apply high-throughput sequencing to confirm the fact that miR-215-5p could be transfered from metastatic ovarian tumor cells to ovarian carcinoma cells in situ. Cell biological techniques in vivo as well as in vitro are employed to prove that miR-215-5p in exosomes targets RADX specifically. Then we verify the essential role RADX plays in DNA damage repair. Finally, combined Co-IP with MS, we detect the downstream regulator A combining with RADX at the DNA damage point. In addition, we affirm the dependance of RADX function on A. The study reveals that RADX deficiency could partly restore the resistance of BRCA2-silencing cells to PARP inhibitor Olaparib, thus providing expeimental evidence for PARP inhibitor targeted therapy in clinical use.