肝癌转移复发是影响其预后的主要因素，最近研究表明转移前微环境中的转移起始细胞是启动转移的关键因素，骨髓来源的内皮祖细胞是转移前微环境中的重要组分也是启动转移的开关。我们前期研究表明Periostin（POSTN）在肝癌中的表达与内皮祖细胞集落数目呈正相关，且POSTN高表达细胞具有肝癌干细胞的特性，然而在转移前微环境中POSTN高表达肝癌细胞能否通过与内皮祖细胞的相互作用转变为转移起始细胞尚未明确。本研究中我们拟利用分子生物学实验及细胞共培养、裸鼠原位共移植、POSTN转基因及基因敲除小鼠自发性肝癌模型等手段，从分子、细胞及活体水平验证转移前微环境中POSTN/CCL2/CD36轴可促使肝癌细胞转变为CD36阳性的转移起始细胞。通过本研究旨在进一步明确POSTN在肝癌转移过程中的作用，并为以POSTN/CCL2/CD36轴为靶点的肝癌抗转移复发治疗提供可靠的理论依据及详实的临床前期数据。

Recurrence and metastasis are the main factors influencing the prognosis of liver cancer. Recent studies have shown that metastasis-initiating cells is the key factor to initiate the metastasis process in pre-metastatic niche. Bone marrow-derived endothelial progenitor cells（EPCs）is an important composition in pre-metastatic microenvironment and it act as a switch in this niche. Our previous studies indicated that there have a positive correlation between the Periostin (POSTN) expression level and the colony numbers of EPCs in hepatocellular carcinoma, and high expression of POSTN liver cancer cells with the characteristics of liver cancer stem cells. However, it is not clear whether high expression of POSTN liver cancer cells could transfer to liver metastasis-initiating cells by interacting with EPCs in pre-metastatic niche. In this study, by using a variety of molecular biology experiment and cell co-culture, orthotopic xenograft with co-transplantation into nude mice, POSTN transgenic and knockout mice model with spontaneous hepatocarcinogenesis method, we would test the hypothysis that control the POSTN/CCL2/CD36 axis in pre-metastatic niche could transfer high POSTN expressed liver cancer cells into CD36 positive metastasis-initiating cells. The purpose of this study is to further clarify the role of POSTN played in the metastasis of liver cancer and furthermore, provide a theoretical basis and reliable preclinical data by targeting POSTN/CCL2/CD36 axis as an anti-metastatic therapy strategy of liver cancer.