PRL-3是诱导结肠癌上皮间质化（EMT）的磷酸酶，EMT则是结肠癌发生肝转移的重要分子作用机制。前期研究证实PRL-3可趋化肿瘤相关性巨噬细胞（TAM）浸润从而使其分泌IL-6和IL-8进而诱导结肠癌EMT的发生，但具体作用机制尚不清楚。预实验证实PRL-3可上调结肠癌细胞CCL-26的表达，TAM细胞可表达CCL-26受体CCR3，提示CCL-26可能参与了PRL-3诱导TAM的浸润过程，由此我们提出假说:PRL-3上调结肠癌细胞CCL-26的表达从而趋化TAM浸润进而诱导结肠癌发生肝转移。本研究拟通过CHIP-PCR、构建荧光素酶载体等技术进一步探讨PRL-3上调CCL-26表达的分子机制，通过细胞共培养、动物实验等探讨CCL-26趋化以及诱导TAM分泌IL-6和IL-8促进结肠癌肝转移的分子信号通路。本研究旨在完善PRL-3促进结肠癌肝转移的作用机制，为结肠癌肝转移治疗提供新靶点。

Phosphatase of regenerating liver-3(PRL-3) is a key phosphotase which induces epithelial-mesenchymal transitions (EMT) of cacer cells and the EMT is the major mechanism by which PRL-3 promotes the liver metastasis of colon cancer. Our research firstly confirm that PRL-3 can induce the infiltration of tumor-associated macrophages (TAM) to secrete cytokines IL-6 and IL-8 leading to the EMT of colon cancer cells in tumor microenvironment. However, the mechanism is still unknown. Our preliminary study has revealed PRL-3 induces the CCL-26 expression of colon cells and the surface of TAM can also express CCL-26 sepecific receptor CCR3. Thus, we firstly propose a new hypothesis that PRL-3 induces the colon cancer cells liver metastasis through the infiltration of TAM in a CCL-26-dependent manner. In this research, we will futher explore the mechanism by which PRL-3 induces the CCL-26 expression through CHIP-PCR and Dual-Luciferase Reporter Assay System methods. Cell co-cultured method and animal experiments are also used to find the key signal pathways which are response for the infiltration of TAM and secretion of TAM-derived IL-6 and IL-8. The study is expected to clarify the novel mechanism by which the PRL-3 promote the colon cancer liver metastasis and find new targets for the treatment of colon cancer liver metastasis.