肿瘤炎症微环境诱导的血管生成对肝癌转移至关重要。有研究证实BRD7在肿瘤炎症微环境和肿瘤转移中发挥作用，但与肝癌微环境诱导的血管生成和转移关系尚不明确。我们前期研究发现BRD7在肝癌组织表达明显下调，与临床TNM分期、门静脉癌栓及肿瘤微血管形成呈负相关，且抑制肝癌细胞的迁移侵袭，提示BRD7具有抑制肝癌转移作用；进一步分析发现该作用可能与BRD7负性调节肿瘤相关中性粒细胞的促血管生成功能有关。目前关于BRD7通过负性调节肿瘤相关中性粒细胞介导的血管生成抑制肝癌转移的具体机制尚不清楚。因此，本项目拟继续研究BRD7在肝癌转移中的具体作用，以及负性调节肿瘤相关中性粒细胞促血管生成的分子机制，并通过小鼠肝癌转移模型探讨BRD7负调控肿瘤相关中性粒细胞介导的血管生成对肝癌转移的影响，以期阐明BRD7抑制肝癌炎症微环境诱导的血管生成和肿瘤转移的作用机制，为将来发展肝癌转移新治疗策略提供理论依据。

Tumor inflammation microenvironment-induced angiogenesis is essential for hepatocellular carcinoma (HCC) metastasis. Recent studies have demonstrated that BRD7 plays a critical role in tumor inflammation microenvironment and tumor metastasis. However, the relationship of BRD7 with tumor microenvironment-induced angiogenesis and metastasis in HCC remains unclear. Our previous studies showed that BRD7 expression was significantly down-regulated in HCC tissues, and BRD7 expression was negatively correlated with clinical TNM staging, portal vein tumor thrombosis, and tumor angiogenesis. In addition, we found that BRD7 could suppress HCC cells migration and invasion. These findings suggested that BRD7 can inhibit HCC metastasis. Further analysis revealed that the effect of BRD7 might be associated with negative regulation of tumor-associated neutrophils(TANs)-induced angiogenesis by BRD7. Currently, the specific mechanism of BRD7 inhibiting HCC metastasis by negatively regulating TANs-mediated angiogenesis is unknown. In this project, we therefore plan to identify the specific effect of BRD7 on HCC metastasis, and investigate the molecular mechanism of BRD7 negatively regulating TANs-induced angiogenesis. We will also establish a mouse model of HCC to explore the effect of BRD7 negatively regulating TANs-mediated angiogenesis on tumor metastasis, thus elucidating the mechanisms in how BRD7 inhibit HCC inflammation microenvironment-induced angiogenesis and tumor metastasis, and providing theoretical basis to develop new treatment strategies for HCC metastasis.