肿瘤微环境在肿瘤转移中的作用日益受到重视，肿瘤微环境是由肿瘤细胞、间质细胞及细胞因子等构成。微环境中炎症因子（含趋化因子）及其受体，如TNF-α、IL-8、CXCL5、CXCL12、CXCR4等，通过复杂的网络化调控，影响着肿瘤的生长、凋亡、血管生成和转移。我们前期研究了TNF-α调控IL-8分泌的机制，预实验发现趋化因子CXCL5在肝癌高转移潜能细胞株中表达显著升高，其分泌亦受TNF-α的诱导。本课题旨在研究CXCL5/CXCR2对肝癌生长转移的作用及机理；CXCL5/CXCR2对TNF-α诱导IL-8分泌的交互作用及反馈调节机制；并利用高通量基因芯片和现代生物信息学技术，构建趋化因子相互作用网络，明确CXCL5或其他关键趋化因子的临床预后价值。本研究有可能发现新治疗靶点和新预后指标。

Nowadays, tumor microenvironment, consisting of tumor cells, stroma cells and cytokines, has been highlighted in tumor metastasis. The Inflammatory cytokines (including chemokines) and their receptors, such as TNF-α、IL-8、CXCL5、CXCL12、CXCR4, affect the tumor growth, apoptosis, angiogenesis and metastasis through complex network regulation. Our previous study elaborated the mechanism of IL-8 production induced by tumor necrosis factor-α in HCC cell lines and found the expression of CXCL5 significantly elevated in HCC cell lines with high metastasis potential, which could also be stimulated by TNF-α. Our research here aims to illustrate the role of CXCL5/CXCR2 in HCC growth and metastasis and its mechanism of cross-talk and feedback with IL-8 induced by TNF-α. Using high through-put gene chips and modern bio-informatic technology, our research also expects to construct chemokines interaction network and to clarify the clinic prognosis value of CXCL5 or other key chemokines. This project also makes it possible for the discovery of new therapy targets and prognosis indicators.