Hypoxia promotes the progression of hepatocellular carcinoma. However, the hypoxia regulatory network in hepatocellular carcinoma is known to be limited. Thus, this study aimed to identify the crucial hypoxia-associated genes and to explore their effects and molecular mechanisms in hepatocellular carcinoma cells. FUT11 was first identified as a crucial hypoxia-associated gene through bioinformatics analysis. High FUT11 mRNA levels were positively correlated with poor clinical parameters. FUT11 knockdown under normoxia and hypoxia both decreased hepatocellular carcinoma cell proliferation, colony formation, migration, and invasion. HIF1α binds to the promoter of FUT11 and increases its transcription and co-expression with FUT11 in hepatocellular carcinoma tissues. Overexpression of FUT11 in HIF1α knockdown cells reversed the inhibitory effects of HIF1α suppression on hepatocellular carcinoma cell proliferation and mobility under hypoxia. Therefore, our findings indicate that FUT11 is a key target gene of HIF1α, which can promote the proliferation and mobility of hepatocellular carcinoma cells. FUT11 may be a novel and effective target for blocking the hypoxia response of hepatocellular carcinoma cells.

中文翻译：

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FUT11是促进肝细胞癌进展的HIF1α靶基因

缺氧促进肝细胞癌的进展。然而，已知肝细胞癌中的缺氧调节网络是有限的。因此，本研究旨在鉴定关键的缺氧相关基因，并探索它们在肝细胞癌细胞中的作用和分子机制。通过生物信息学分析， FUT11首次被确定为关键的缺氧相关基因。高 FUT11 mRNA 水平与较差的临床参数呈正相关。在常氧和缺氧条件下敲低FUT11均降低了肝癌细胞的增殖、集落形成、迁移和侵袭。HIF1α 与FUT11的启动子结合并增加其转录和与FUT11的共表达在肝细胞癌组织中。HIF1α敲低细胞中FUT11的过表达逆转了HIF1α抑制对缺氧条件下肝细胞癌细胞增殖和迁移的抑制作用。因此，我们的研究结果表明，FUT11是HIF1α的关键靶基因，可以促进肝癌细胞的增殖和迁移。FUT11可能是阻断肝癌细胞缺氧反应的新型有效靶点。