G蛋白偶联受体家族（GPCR）作为肿瘤及其他疾病的靶向治疗的明星分子，一直是药物研发中最广泛应用的药物靶点。本研究以肝癌免疫微环境在肝癌的发生发展中的重要作用为出发点，基于炎癌转化观念，重点关注GPCR在肝癌免疫微环境及其所介导的肿瘤细胞恶性行为。通过高通量芯片及GPCR数据库筛选获得在肝癌免疫微环境T细胞中具有重要作用的CD97分子，借助同源建模技术从蛋白3D结构预测其下游信号通路，并通过体外炎、癌细胞共培养，体内肿瘤生长模型，共同分析CD97及其介导的信号通路在免疫细胞中异常激活时效应及机制。本课题旨在从炎症角度以GPCR为靶标更好的诠释肝癌发生，为肝癌未来组合药物靶标的鉴定奠定理论基础。

G-protein-coupled receptors (GPCR) is regarded as the famous star of molecular targeted therapy of cancer and other diseases, and has been the most widely used drug targets for drug development. In this study, based on the important function of immune microenvironment in the development of hepatocellular carcinoma(HCC), we focused on the GPCR involved in HCC according to the inflammation induced cancer theory. High-throughput chipsets screening combined with GPCR database was applied to screen the associated GPCR in T cell infiltrated in liver cancer, among which, CD97 was screened as candidate after the loss and gain of function assays. Homologous 3D modeling was also employed to identify possible target signaling network for CD97. Verification and correlation tests on some key molecules within this network will be carried out based on amount of clinical samplers, moreover, the impact of CD97 abnormality on the malfunction of tumor infiltrating immunocytes will be further evaluated. The role of abnormal activation of CD97 signaling network in tumor infiltrating immunocytes on development of HCC will be explored by a serial of experiments including in vitro co-culture of inflammatory and liver cancer cells, in vivo tumor growth mice hepatocarcinogenesis models. The outcomes of this project will lay the theoretical foundation for a better interpretation of inflammation related hepatocarcinogenesis.