提高肝癌治愈率的关键仍在于早诊断和早治疗。新近研究开始聚焦于从细胞分子层面来探讨肝细胞肝癌（HCC）的发病机制，以期能找到新的早期诊疗靶标。前期研究我们知道，PLK1激酶通过磷酸化下游底物cdc25c、cdc25A、Emi1等，参与调控细胞增殖、周期、凋亡、迁移等一系列生物学功能，在HCC发生发展过程中发挥重要作用。这提示PLK1是潜在的HCC靶标分子。而另一些研究则表明，HCC发生发展进程中伴随miRNAs的参与及调控。本研究通过筛选得到参与调控PLK1表达的miRNA，即miR-296-5p，探讨其调控机制，以明确其对HCC细胞增殖、周期、凋亡、迁移及侵袭情况影响；并构建裸鼠HCC模型，检测miR-296-5p/PLK1对裸鼠皮下成瘤能力影响及原位肝脏移植瘤转移能力影响。本课题为HCC的发病机制提供新的理论基础，为预防和治疗HCC提供新的靶点及诊疗指标。

The key to improve the cure rate of liver cancer is still in the early diagnosis and early treatment. Recent studies have begun to focus on the cellular and molecular level to explore the pathogenesis of hepatocellular carcinoma (HCC), in order to find new early diagnosis and treatment targets. Previous studies we know that PLK1 kinase phosphorylation by downstream substrates cdc25C, cdc25A and Emi1, participate in the regulation of cell proliferation, cell cycle, apoptosis, migration, and a series of biological functions, play an important role in the process of development of HCC. This suggests that PLK1 is a potential HCC target molecule. While other studies show that HCC is involved in the development and regulation of miRNAs. In this study, we screened miRNAs involved in the regulation of Plk1 expression, and find miR-296-5p. We then explore the regulation mechanism, in order to make clear how it influence HCC cell proliferation, cell cycle, apoptosis, migration and invasion of influence. And we will construct nude mouse model of HCC, detection miR-296-5p/PLK1 on the nude mice tumorigenicity ability and orthotopic liver transplantation tumor metastasis affected. This topic provides a new theoretical basis for the pathogenesis of HCC, to provide a new target and diagnostic targets for the prevention and treatment of HCC.