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Abstract：
BACKGROUND: Gastric cancer (GC) is a malignant digestive tract tumor with a high recurrence rate and poor prognosis. Fucosylation is important in tumor glycosylation, in which the key enzyme is fucosyltransferase (FUT). FUT11 is a member of the fucosyltransferase family and has been closely associated with the development of multiple cancers. However, the specific relationship between FUT11 and GC prognosis and its molecular mechanism has not been fully studied. This study explored FUT11 expression, clinical correlation, and its role in GC occurrence and development to deepen understanding of its function.
METHODS: FUT11 expression in 33 cancers was preliminarily analyzed using the Tumor Immunoassay Resource (TIMER2.0) database. FUT11 expression in GC was evaluated using The Cancer Genome Atlas stomach adenocarcinoma (TCGA-STAD) and Gene Expression Profiling Interactive Analysis (GEPIA2) data and verified using the Gene Expression Omnibus (GEO) GSE65801 dataset. Furthermore, we studied the survival prognosis of FUT11 in GC and analyzed its effect on the survival rate of patients with GC using the KM-plotter. We also performed COX regression analysis on TCGA GC clinical data and analyzed FUT11 expression in the pathway using the STRING and LinkedOmics databases. Moreover, the relationship between FUT11 and GC immune infiltration level was examined, and the Kaplan-Meier survival analysis diagram was constructed. The FUT11 genetic variation information was retrieved using cBioPortal, and its drug sensitivity was analyzed using CellMiner. Finally, differential FUT11 expression in GC tissues was verified using immunohistochemistry.
RESULTS: The data mining and analysis demonstrated that FUT11 expression was abnormally elevated in GC tissues and correlated with poor patient prognosis. The FUT11 expression level was an independent prognostic factor for GC. The difference in FUT11 expression level resulted in different degrees of immune cell infiltration in the patients with GC, which might regulate the tumor microenvironment. FUT11 affected GC development by participating in cancer pathways such as PI3K-AKT, neuroactive ligand-receptor, and MAPK. Immunohistochemical staining revealed that FUT11 was highly expressed in GC.
CONCLUSIONS: This study revealed that FUT11 expression is significantly increased in GC tissues. This increase is associated with poor prognosis and might affect immune regulation. FUT11 might have immunological and targeted therapeutic value, providing a new approach to GC treatment.
METHODS: FUT11 expression in 33 cancers was preliminarily analyzed using the Tumor Immunoassay Resource (TIMER2.0) database. FUT11 expression in GC was evaluated using The Cancer Genome Atlas stomach adenocarcinoma (TCGA-STAD) and Gene Expression Profiling Interactive Analysis (GEPIA2) data and verified using the Gene Expression Omnibus (GEO) GSE65801 dataset. Furthermore, we studied the survival prognosis of FUT11 in GC and analyzed its effect on the survival rate of patients with GC using the KM-plotter. We also performed COX regression analysis on TCGA GC clinical data and analyzed FUT11 expression in the pathway using the STRING and LinkedOmics databases. Moreover, the relationship between FUT11 and GC immune infiltration level was examined, and the Kaplan-Meier survival analysis diagram was constructed. The FUT11 genetic variation information was retrieved using cBioPortal, and its drug sensitivity was analyzed using CellMiner. Finally, differential FUT11 expression in GC tissues was verified using immunohistochemistry.
RESULTS: The data mining and analysis demonstrated that FUT11 expression was abnormally elevated in GC tissues and correlated with poor patient prognosis. The FUT11 expression level was an independent prognostic factor for GC. The difference in FUT11 expression level resulted in different degrees of immune cell infiltration in the patients with GC, which might regulate the tumor microenvironment. FUT11 affected GC development by participating in cancer pathways such as PI3K-AKT, neuroactive ligand-receptor, and MAPK. Immunohistochemical staining revealed that FUT11 was highly expressed in GC.
CONCLUSIONS: This study revealed that FUT11 expression is significantly increased in GC tissues. This increase is associated with poor prognosis and might affect immune regulation. FUT11 might have immunological and targeted therapeutic value, providing a new approach to GC treatment.
摘要：
背景：胃癌是一种恶性消化道肿瘤，复发率高，预后差。岩藻糖基化在肿瘤糖基化中起重要作用，其中关键酶是岩藻糖基转移酶(FUT)。FUT11是岩藻糖基转移酶家族的一员,与多种癌症的发生发展密切相关。然而,FUT11与GC预后的具体关系及其分子机制尚未得到充分研究。本研究探讨了FUT11的表达，临床相关性，以及其在GC发生发展中的作用,加深对其功能的认识。
方法：使用肿瘤免疫分析资源（TIMER2.0）数据库初步分析了33种癌症中FUT11的表达。使用癌症基因组图谱胃腺癌(TCGA-STAD)和基因表达谱交互分析(GEPIA2)数据评估GC中的FUT11表达,并使用基因表达综合(GEO)GSE65801数据集进行验证。此外，我们研究了FUT11在GC中的生存预后，并使用KM绘图仪分析了其对GC患者生存率的影响。我们还对TCGAGC临床数据进行了COX回归分析，并使用STRING和LinkedOmics数据库分析了该途径中的FUT11表达。此外，检测FUT11与GC免疫浸润水平的关系,构建了Kaplan-Meier生存分析图。使用cBioPortal检索了FUT11遗传变异信息，并使用CellMiner分析其药物敏感性。最后,使用免疫组织化学验证了GC组织中差异的FUT11表达。
结果：数据挖掘和分析表明，FUT11在GC组织中表达异常升高，与患者预后不良相关。FUT11表达水平是GC的独立预后因素。FUT11表达水平的差异导致GC患者不同程度的免疫细胞浸润,这可能会调节肿瘤微环境。FUT11通过参与PI3K-AKT等癌症通路影响GC发展，神经活性配体受体，和MAPK。免疫组织化学染色显示FUT11在GC中高表达。
结论：本研究显示FUT11在GC组织中的表达显著增加。这种增加与不良预后有关，并可能影响免疫调节。FUT11可能具有免疫学和靶向治疗价值，为GC治疗提供了新的途径。
方法：使用肿瘤免疫分析资源（TIMER2.0）数据库初步分析了33种癌症中FUT11的表达。使用癌症基因组图谱胃腺癌(TCGA-STAD)和基因表达谱交互分析(GEPIA2)数据评估GC中的FUT11表达,并使用基因表达综合(GEO)GSE65801数据集进行验证。此外，我们研究了FUT11在GC中的生存预后，并使用KM绘图仪分析了其对GC患者生存率的影响。我们还对TCGAGC临床数据进行了COX回归分析，并使用STRING和LinkedOmics数据库分析了该途径中的FUT11表达。此外，检测FUT11与GC免疫浸润水平的关系,构建了Kaplan-Meier生存分析图。使用cBioPortal检索了FUT11遗传变异信息，并使用CellMiner分析其药物敏感性。最后,使用免疫组织化学验证了GC组织中差异的FUT11表达。
结果：数据挖掘和分析表明，FUT11在GC组织中表达异常升高，与患者预后不良相关。FUT11表达水平是GC的独立预后因素。FUT11表达水平的差异导致GC患者不同程度的免疫细胞浸润,这可能会调节肿瘤微环境。FUT11通过参与PI3K-AKT等癌症通路影响GC发展，神经活性配体受体，和MAPK。免疫组织化学染色显示FUT11在GC中高表达。
结论：本研究显示FUT11在GC组织中的表达显著增加。这种增加与不良预后有关，并可能影响免疫调节。FUT11可能具有免疫学和靶向治疗价值，为GC治疗提供了新的途径。
