ZYX36-58是我们前期通过质谱筛选获得的、在正常组织中丰度较高、在高级别浆液性腺癌肿瘤组织与高转移卵巢癌细胞HO8910PM中丰度均极低的一条多肽，前期我们初步证实ZYX36-58具有抑制卵巢癌侵袭转移功能，利用pull down等实验发现ZYX36-58可能通过结合NEDD9发挥作用。既往文献提示NEDD9主要通过结合黏着斑激酶和SRC等调节细胞的侵袭迁移等，其表达水平与卵巢癌FIGO分期呈正相关，是卵巢癌极具潜力的治疗靶标。因此，为论证ZYX36-58作为卵巢癌治疗潜在分子的可行性，本研究拟从细胞及动物模型水平进一步评估ZYX36-58对人卵巢癌细胞侵袭转移的作用，并通过Rescue策略论证ZYX36-58通过NEDD9介导的作用机制。目前尚无ZYX36-58的报道，本研究将揭示ZYX36-58抑制卵巢癌侵袭迁移的作用与机制，为卵巢癌治疗和药物研发提供新线索。

ZYX36-58 is an endogengous peptide identified by mass spectrometry. Its aboudance is high in ovarian cancer adjacent tissue and low in High Grade Ovarian adenocarcinoma as well as the highly metastatic ovarian cancer cell line, HO8910PM. Our previous study indicated that ZYX36-58 can inhibit cell invasion and migration in vitro and in vivo. Besides, we found NEDD9 as a potential target of ZYX36-58 by pull down assay, which regulates cell invasion and migration through binding of focal adhesion kinase and SRC. Previous study indicated that a high level of NEDD9 expression is significantly correlated with advanced stage tumors and high grade carcinomas and NEDD9 may serve as a potential target of ovarian cancer. To further evaluate the possibility of ZYX36-58 as an ovarian cancer therapeutic target, we will further investigate the inhibit effect of ZYX36-58 on ovarian cancer cell invasion and migration in vitro and in vivo and explore the mechanism of ZYX36-58 function through NEDD9. So far there is no report of ZYX36-58, our study will is of certain novelty and will provide new clue for the therapeutic of ovarian cancer.