肝细胞癌（HCC）作为最常见的消化系统恶性肿瘤之一，致死率高，严重威胁人类生命和健康，目前对HCC发生发展的分子机制了解仍不全面。课题前期通过芯片筛选和基因表达检测发现，miR-224-5p在HCC组织中表达上调，进一步通过生物信息预测发现，circRNA CCND1与RECK存在相同的miR-224-5p应答元件，且都在HCC进程中异常表达，RECK基因具有抑制MMPs类蛋白发挥抑癌的功能，但三者之间在HCC中的功能及机制不清楚。因此提出circRNA CCND1可作为ceRNA吸附竞争miR-224-5p介导RECK基因发挥抑癌作用，从而参与HCC发生发展的假说。本课题拟从细胞和动物模型两个层面研究HCC中circRNA CCND1、miR-224-5p和RECK之间的作用关系，揭示circRNA CCND1/miR-224-5p/RECK轴的抑癌作用以及其在HCC中的功能机制。

Hepatocellular carcinoma (HCC), as one of the most common malignant tumors of the digestive system, is under a high fatality rate and seriously threatens human life and health. At present, the molecular mechanism of HCC development is still not fully appreciated. In the early stage of the project, through chip screening and gene expression detection, it was found that the expression of miR-224-5p was up-regulated in HCC tissues, and further through biological information prediction, it was found that the same miR-224-5p response element exists in circRNA CCND1 and RECK, and both are in the HCC process Abnormal expression in RECK gene has the function of inhibiting MMPs to exert tumor suppressive function, but the function and mechanism of the three in HCC are unclear. Therefore, it is proposed that circRNA CCND1 can serve as a ceRNA adsorption competition miR-224-5p mediated RECK gene plays a tumor suppressor role, thereby participating in the hypothesis of HCC development. This subject is intention to study the relationship between circRNA CCND1, miR-224-5p and RECK in HCC from two levels of cell and animal models, revealing the tumor suppressive effect of circRNA CCND1/miR-224-5p / RECK axis and its role in HCC Functional mechanism.