肝细胞癌是目前最常见的威胁人类生命的疾病之一，是全球第五大高发和第三致死性的恶性肿瘤。RACK1是一个高度保守的构架蛋白，在信号传导和肿瘤发生过程中发挥重要的作用。有研究提示RACK1是核糖体40S小亚基的组成部分并与核糖体RNA直接作用；我们最近报道发现，核糖体RACK1能够通过蛋白质翻译调控来促进肝细胞癌的生长和化疗抵抗。然而，肝细胞癌中核糖体RACK1的功能如何被调控并没有相关报道。在本项目中，我们首次对O-GlcNAc糖基化修饰在调控核糖体RACK1功能中的作用进行了研究。我们拟鉴定核糖体RACK1的O-GlcNAc糖基化修饰并探讨修饰的调控机制，同时研究O-GlcNAc修饰对核糖体RACK1的功能调控和分子机制，以期阐明肝细胞癌中O-GlcNAc糖基化修饰在核糖体RACK1调控蛋白质翻译和促进肿瘤过程的重要作用，为研究O-GlcNAc修饰在肝细胞癌中的功能提供新的线索。

Hepatocellular carcinoma (HCC) is among the most common and lethal cancers in the human population, ranked the fifth most frequent neoplasm and the third most common cause of cancer-related death worldwide. Receptor for activated C-kinase 1 (RACK1) is a highly-conserved scaffold protein, and plays a pivotal role in signal transduction and tumor progression. Previous studies show that RACK1 is a component of the 40S small subunit of ribosome and directly interacts with ribosomal RNA; we also have reported that ribosomal RACK1 promotes the growth and chemoresistance of HCC through translational regulation. However, what modulates the tumorigenic role of ribosomal RACK1 in HCC is little understood. In this study, we examine the role of O-GlcNAc modification in modulating the tumorigenic impact of ribosomal RACK1 for the first time. We will identify the O-GlcNAc modification of ribosomal RACK1 as well as the regulating mechanism. We also will examine the effect of O-GlcNAc modification on ribosomal RACK1 and the underlying mechanism, thus elucidating the role of O-GlcNAc modification in ribosomal RACK1-mediated translational regulation and HCC progression and providing new clues to understanding the role of O-GlcNAc modification in HCC.