胰腺癌发病隐匿、发展迅速，缺乏有效治疗手段。EGFL7是新近发现的促血管生成因子，结构类似Notch信号通路受体的功能区，但其在胰腺癌中的研究鲜有报道。我们前期研究发现胰腺癌患者外周血及肿瘤组织中EGFL7转录激活表达升高，且与疾病进展密切相关。EGFL7抗体阻断下胰腺癌细胞的侵袭能力和促血管生成能力明显减弱。据此提出假说：EGFL7转录激活并可能通过Notch通路参与了胰腺癌的发生发展。本项目拟深入观察EGFL7、Notch信号通路相关基因的表达与胰腺癌临床病理特征的关系，并针对人胰腺癌细胞及动物模型，运用基因沉默和过表达手段靶向调节EGFL7的表达，适时阻断Notch通路，从分子、细胞、组织及动物水平观察EGFL7与胰腺癌生长、血管生成、侵袭转移之间的关系，掌握其在胰腺癌发生发展中的规律和手段，探讨相关机制，为EGFL7可能成为胰腺癌基因治疗的潜在靶点提供一定的理论基础和实验依据。

Pancreatic cancer is definitely the most deadly malignant disease in the digestion system, and has no effective treatment. EGFL7 has been discovered recently as an angiogenesis factor,function structure similar to Notch receptors, but has been rarely reported in pancreatic cancer. Our previous study found that increased transcription activation and expression of EGFL7 in peripheral blood and tumor tissue of patients with pancreatic cancer,and is associated with tumor progression. The invasion and angiogenesis ability significantly weakened in pancreatic cancer cells after EGFL7 antibody blocking. Accordingly,we put forward the hypothesis: EGFL7 transcriptional activation is involved in the occurrence and development of pancreatic cancer through the Notch pathway. This project aims to observe the relationship between the EGFL7, Notch signal pathway and clinical pathological features of pancreatic cancer, and according to the human pancreatic cancer cell and animal models, using gene silencing and overexpression targeting the regulation of EGFL7 expression, timely blocking the Notch pathway, make sure the relationship between EGFL7 and the growth,angiogenesis,invasion and metastasis of pancreatic cancer from molecules, cells, tissues and animal levels,master the rules and methods of EGFL7 during the development of pancreatic cancer, explore the relative mechanisms, to provide theoretical and experimental basis for EGFL7 as a potential target to pancreatic cancer gene therapy.