慢性炎症在肝细胞癌（HCC）的发生发展过程中具有促进作用，但具体作用机制尚未完全明确。课题组前期研究发现：RASSF1A的表达异常与HCC的发生发展密切相关，并且能与淋巴毒素β受体（LTβR）相结合，干扰HCC细胞LTβR的表达可消除RASSF1A过表达对HCC细胞生长抑制的影响。因此，我们提出RASSF1A负性调节LTβR信号转导抑制HCC发生发展的假设。本研究将首先明确RASSF1A与LTβR能否结合形成复合物,再分析RASSF1A与LTβR结合对LTβR激活及下游信号的调节作用，接着观察RASSF1A与LTβR结合对HCC细胞体内外生物学行为的影响，最后分析RASSF1A与LTβR的结合与HCC临床病理特征和预后的相关性。本研究结果将为阐明RASSF1A调控HCC发生发展的分子机制提供实验基础，也为HCC的预防和治疗提供新的理论依据。

Chronic inflammation promotes genesis and development of hepatocellular carcinoma (HCC), however the detailed mechanisms is not fully understood yet. Our previous study suggested that the abnormal expression of Ras association domain family 1A (RASSF1A) gene was closely related with genesis and development of HCC, which could bind with lymphotoxin beta receptor (LTβR). The effects of RASSF1A overexpression on HCC cell proliferation could be inhibited by interfering the expression of LTβR in HCC cells. Therefore, we proposed a hypothesis that RASSF1A negatively regulates the signal transduction of LTβR and inhibits the process of HCC. Firstly, this study will demonstrate whether RASSF1A and LTβR can form any compound. And then the regulation role of RASSF1A and LTβR combination in LTβR activation and downstream signal will be analyzed. Furthermore, the effects of RASSF1A and LTβR combination on biological behavior of HCC cells in vitro and in vivo will be investigated. Finally, the correlation between the RASSF1A and LTβR combination and clinical pathological characteristics and prognosis of HCC will be analyzed. This study will provide basic experiments to elucidate the molecular mechanism of RASSF1A in the regulation of genesis and development of HCC, and afford new theoretical basis for the prevention and treatment of HCC.