肿瘤细胞VEGF/VEGFR自分泌环的活化可促进肿瘤细胞增殖、迁移，而抑制此环路具有明显的抗肿瘤作用。OVA66是从人卵巢癌 cDNA文库中筛得的肿瘤相关抗原，在多种肿瘤组织中高表达，并促进肿瘤细胞的增殖和迁移。前期实验发现，干扰OVA66明显抑制卵巢癌和宫颈癌细胞VEGF/VEGFR2信号通路的活化和VEGF分泌，提示OVA66可调控肿瘤细胞VEGF/VEGFR2自分泌环。本课题就其调控作用展开研究：1）深入探讨OVA66 对肿瘤细胞VEGF/VEGFR2自分泌环的调控及机制；2）系统阐明OVA66如何通过VEGF/VEGFR2自分泌环影响肿瘤细胞的生物学行为；3）探究OVA66对VEGF/VEGFR2自分泌环的调控在卵巢癌和宫颈癌中的临床意义。阐明OVA66 对肿瘤细胞VEGF/VEGFR2自分泌环的调控及机制，对靶向VEGF/VEGFR2的抗肿瘤治疗提供新思路和新靶标，具有重要意义。

Activation of VEGF/VEGFR autocrine loop in tumor cell can promote its proliferation and migration potential. Inhibition of VEGF/VEGFR autocrine loop exhibits obvious anti-tumor effects. OVA66 is a tumor associated antigen identified in ovarian carcinoma complementary DNA (cDNA) expression library. It has been indicated OVA66 was overexpressed in a wide variety of human tumor tissues and can promote proliferation and invasion of tumor cells. Previous experiment showed that interference of OVA66 expression significantly inhibited the activation of VEGF/VEGFR2 autocrine loop and VEGF secretion in ovarian and cervical cancer cells, which suggested a role of OVA66 in regulating VEGF/VEGFR2 autocrine loop of tumor cells. Therefore, this project intend to expand the research on this regulating capacity of OVA66: (1) Explore the role and mechanism of OVA66 in regulating VEGF/VEGFR2 autocrine loop of tumor cells; (2) Clarify how OVA66 influence the biological behavior of tumor cells in vitro and in vivo by regulating VEGF/VEGFR2 autocrine loop; (3) Investigate the clinical significance of OVA66 in ovarian cancer and cervical cancer by regulating VEGF/VEGFR2 autocrine loop. It is of great importance to elucidate the regulating role of OVA66 in VEGF/VEGFR2 autocrine loop of tumor cells and its mechanism. The potential findings will help to support new idea and new target for anti-tumor therapy targeting VEGF/VEGFR2 autocrine loop.