PRL-3与结直肠癌发生转移密切相关，但作用机制仍不清楚。本项目拟在前期已成功构建可视化PRL-3(+)/APC(min/+)自发结直肠腺瘤转基因小鼠模型基础上，动态观察转基因小鼠结直肠腺瘤癌变发生及侵袭转移情况，活体内整体水平证实PRL-3过表达在结直肠癌发生发展中的作用；通过原代培养小鼠结直肠腺瘤、癌变组织与转移癌组织，体外实验验证PRL-3对结直肠腺瘤细胞生长、癌变及转移的影响；应用比较基因组学、比较蛋白质组学分析及生物信息学技术，寻找PRL-3过表达后小鼠结直肠腺瘤发生癌变及转移的差异表达基因/蛋白；通过荧光定量PCR、蛋白免疫印迹、免疫共沉淀、免疫荧光共定位分析鉴定与PRL-3相互作用基因/蛋白，筛选PRL-3相关信号通路上结直肠癌发生与转移的关键分子，明确PRL-3在结直肠腺瘤癌变及转移中的作用机制及其相关信号调控网络，为结直肠癌的诊治提供新理论和新靶标。

PRL-3 is closely related to tumorigenesis and metastasis of colorectal cancer, but the mechanism is still unclear. Based on the visualizing PRL-3 (+) / APC (min / +) spontaneous colorectal adenoma transgenic mouse model, this study aims to observe malignancy transformation dynamically, subsequent invasiveness and metastasis, in vivo. After confirming overexpression PRL-3 in transgenic mice, we also validate the effects of PRL-3 on initiating and progression of colorectal cancer de novo. Serial experiments in vitro are attempted to verify PRL-3's role of transformation, growth and metastasis in primary cancer and secondary cancer tissues with tumor cells culture. Differentially expressed genes/ protein will be obtained from DNA microarray, comparative proteomics and bioinformatics analysis between colorectal adenoma, primary cancer and metastasis tissues derived from PRL-3 overexpressed mice then they will be confirmed in quantitative RT-PCR, western blot, co-immunoprecipitation assay and immunofluorescence co-localization analysis. After identifying the key molecules interacted with PRL-3, we propose to illuminate PRL-3 signal pathway in regulating malignancy transformation and progression of colorectal adenoma and provide new theories and new targets for the treatment of colorectal cancer.