从探索卵巢癌腹水中可能存在的保护成分出发，我们利用质谱技术筛选了卵巢癌化疗敏感病人和耐药病人腹水中差异表达的多肽，发现其中敏感病人中丰度较高的CPAP1在体内和体外均可以提高卵巢癌的顺铂敏感性。pull-down实验发现位于卵巢癌铂类耐药相关染色体区域的URI可能是CPAP1的靶基因，CPAP1的加入可以显著抑制顺铂诱导的URI下游S6K1-BAD信号通路的激活，提示CPAP1可能通过靶向URI提高卵巢癌的顺铂敏感性。本研究拟验证CPAP1促顺铂敏感性作用对其他铂类药物的适用性；利用卵巢癌耐药细胞、原位模型和病人来源移植瘤(PDX)模型全面评估CPAP1提高卵巢癌顺铂敏感性的作用；以URI为机制主线，通过物理学方法、挽救实验方案深入阐明CPAP1的作用机制；探索提高CPAP1稳定性和活性的修饰方法。研究如获成功，有望为卵巢癌临床化疗提供新的辅助治疗手段，因此具有较强的创新性和转化前景。

In order to explore the protective molecules in ovarian cancer ascites, we used mass spectrometry to screen differentially expressed peptides in ascites of chemosensitive and chemoresistant ovarian cancer patients. We found that CPAP1 peptide could increase the cisplatin sensitivity of ovarian cancer cells in vivo and in vitro. Peptide pull-down assay found that URI which is located in the chromosomal region associated with platinum-resistance of ovarian cancer may be the target of CPAP1. Cisplatin induced activation of S6K1-BAD signaling pathway downstream of URI was significantly inhibited by adding CPAP1. So we hypothesized that CPAP1 can increase the chemosensitivity of ovarian cancer by targeting URI. In the future, we will verify the applicability of CPAP1 function in promoting cisplatin sensitivity to other platinum drugs, and comprehensively evaluated the CPAP1 function in promoting cisplatin sensitivity of ovarian cancer by using drug-resistant ovarian cancer cells, the ovarian cancer orthotopic model and the Patient Derived Xenograpt (PDX) model, and further elucidated the mechanism of CPAP1 function in increasing the cisplatin sensitivity by physical methods and rescue experiment. Besides, we will explore the modification methods to improve the stability and activity of CPAP1. If the study is successful, it is expected to provide a new adjuvant therapy for ovarian cancer clinical chemotherapy, so it has a strong innovation and transformation application prospects.