Neuropilin-1（NRP-1）被认为是一个很有前景的癌症治疗靶点，它是一个多功能细胞表面受体。课题组前期成功制备鉴定Anti-NRP-1mAb，初步探讨其抑制乳腺癌细胞增殖、迁移和粘附机理。但关于NRP-1在乳腺癌新生淋巴管形成和淋巴结转移中的作用和机制，目前尚不清楚。本项目拟以转移性乳腺癌MDA-MB-231为研究对象，通过干扰NRP-1表达或抑制NRP-1功能，观察NRP-1在调控乳腺癌新生淋巴管形成和转移过程中的作用。同时通过分析NRP-1与PI3K、AKT、VEGFR-3及integrinαvβ3的蛋白和mRNA表达的相关性，阐明NRP-1通过PI3K/AKT信号通路调控乳腺癌淋巴管生成和淋巴结转移的作用机制，为基于NRP-1靶点的肿瘤靶向治疗提供新策略和理论依据。

Neuropilin-1(NRP-1) is regarded as a promising target for cancer therapy.It is a non-tyrosine kinase receptor for semaphorin 3A(Sema 3A) and vascular endothelial growth factor(VEGF) involved in tumor angiogenesis, growth and metastasis.In preparatory study，the anti-NRP-1mAb was obtained and the affinity of antibody was identified. It can inhibits the adhesion of breast cancer cell MCF7 to fibronectin by suppressing FAK/p130cas signaling pathway. In this study，we aim to investigated the effects of NRP-1 to tumor cells proliferation, migration and adhesion in breast cancer MDA-MB-231 after treatment with anti-NRP-1mAb or NRP-1 RNAi, respectively. To asssay differention of the migration by boyden chamber and canaliculization by culture with MDA-MB-231 cells. To observe the tumor growth, metastasis and lymphangiogenesis in nude mice, Also to detect the expression of NRP-1, PI3K, AKT, VEGFR-3 and integrin αvβ3. Finally, to illuminate the regulation mechanism of lymphangiogenesis and metastasis in breast Cancer by NRP-1 through PI3K/AKT signaling pathway which may be a importent theory basis that the Anti-NRP-1mAb is likely to be a prospective antibody drug candidate for tumor treatment.