Asparagine-linked glycosylation protein 1同源物(ALG1)参与蛋白质N-糖基化的初始阶段，而N-糖基化与肝细胞癌(HCC)的进程有关。然而，ALG1在人类HCC中是否有作用仍不清楚。本研究分析了肿瘤和相应的相邻非肿瘤组织中ALG1的表达谱，并使用免疫组化方法评估了ALG1表达与HCC患者临床特征和预后之间的关系。我们发现，与相邻的正常肝组织相比，HCC组织中ALG1的表达降低，这预示着不利的预后。结合RNA干扰，我们系统地确定了Huh7细胞系中新生蛋白质组和糖蛋白质组。生物信息学分析表明，在ALG1敲低响应中不同表达的蛋白质与细胞间粘附最相关。功能研究证实，ALG1的敲低降低了细胞粘附能力，促进了细胞迁移。此外，我们还发现在N-钙黏蛋白上H8N2（在N-糖基化位点N651）和H5N4S2F1（在N-糖基化位点N692）的下调是ALG1敲低的特征。我们的发现揭示了ALG1控制糖基化的N-钙黏蛋白的表达，并在HCC迁移中发挥作用，这对预后具有意义。在线版本包含可在10.1007/s43657-022-00050-5获取的补充材料。©国际人类表型研究所（上海）2022。

Asparagine-linked glycosylation protein 1 homolog (ALG1) participates in the initial stage of protein N-glycosylation and N-glycosylation has been implicated in the process of hepatocellular carcinoma (HCC) progression. However, whether ALG1 plays a role in human HCC remains unknown. In this study, the expression profile of ALG1 in tumorous and corresponding adjacent non-tumor tissues was analyzed. The relationship of ALG1 expression with clinical features and prognosis of HCC patients was also evaluated using immuno-histochemical method. Here we found ALG1 decreased in HCC tissues compared with adjacent normal liver tissues, which predicted an unfavorable prognosis. Combined with RNA interference, nascent proteome and glycoproteome were determined systematically in Huh7 cell line. Bioinformatics analysis indicated that the differentially expressed proteins participating in the response of ALG1 knockdown were most significantly associated with cell-cell adhesion. Functional studies confirmed that knockdown of ALG1 reduced cell adhesion capacity, and promoted cell migration. Furthermore, down-regulation of H8N2 (on N-glycosite N651) and H5N4S2F1 (on N-glycosite N692) from N-cadherin was identified as a feature of ALG1 knockdown. Our findings revealed that ALG1 controlled the expression of glycosylated N-cadherin and played a role in HCC migration, with implications for prognosis.The online version contains supplementary material available at 10.1007/s43657-022-00050-5.© International Human Phenome Institutes (Shanghai) 2022.