Abstract：
The association between SLC10A3 (solute carrier family 10 member 3) and lower grade glioma (LGG) remains unclear.
We used public databases and bioinformatics analysis to analyze SLC10A3. These included The Cancer Genome Atlas, Genotype-Tissue Expansion, Chinese Glioma Genome Atlas, Human Protein Atlas, GeneCards, cBioPortal, Search Tool for the Retrieval of Interacting Genes/Proteins, Gene Expression Profiling Interactive Analysis, Tumor Immune Estimation Resource, Tumor-Immune System Interaction Database, receiver operating characteristic curve analysis, Kaplan-Meier analysis, Cox analysis, nomograms, calibration plots, gene ontology/Kyoto Encyclopedia of Genes and Genomes enrichment analysis, gene set enrichment analysis, single-sample gene set enrichment analysis, and Spearman\'s correlation analysis.
SLC10A3 was upregulated in adrenocortical carcinoma, glioblastoma, and LGG and was associated with good overall survival (OS) in adrenocortical carcinoma and poor OS in LGG and glioblastoma. SLC10A3 was increased with increased World Health Organization grade, upregulated in isocitrate dehydrogenase-wild type, 1p/19q (chromosome arms 1p and 19q) non-co-deleted, and higher in astrocytoma. Patients with LGG were grouped by the occurrence of the clinical outcome endpoints (i.e., OS, disease-specific survival [DSS], and progression-free interval events). Genetic alterations in SLC10A3 were associated with poor progression-free survival in LGG. Most of clinical characteristics were associated with the SLC10A3 expression level. SLC10A3 with diagnostic and prognostic value (OS, DSS, and progression-free interval) was an independent prognostic factor in LGG. Moreover, Nomograms (WHO grade, 1p/19q codeletion, age and SLC10A3) had moderately accurate predictive for OS and DSS. Functional analysis showed that SLC10A3 might participate in the transport of multiple substances, neurogenic signaling, immune response, and programmed cell death in LGG. SLC10A3 correlated with immune infiltration in LGG and moderately correlated with the gene signature of pyroptosis, lysosome-dependent cell death, necroptosis, apoptosis, ferroptosis, alkaliptosis, and autophagy-dependent cell death.
SLC10A3 is a potential diagnostic and prognostic biomarker for LGG and might be associated with substance transport, neurogenic signaling, immune infiltration, and programmed cell death in LGG.
We used public databases and bioinformatics analysis to analyze SLC10A3. These included The Cancer Genome Atlas, Genotype-Tissue Expansion, Chinese Glioma Genome Atlas, Human Protein Atlas, GeneCards, cBioPortal, Search Tool for the Retrieval of Interacting Genes/Proteins, Gene Expression Profiling Interactive Analysis, Tumor Immune Estimation Resource, Tumor-Immune System Interaction Database, receiver operating characteristic curve analysis, Kaplan-Meier analysis, Cox analysis, nomograms, calibration plots, gene ontology/Kyoto Encyclopedia of Genes and Genomes enrichment analysis, gene set enrichment analysis, single-sample gene set enrichment analysis, and Spearman\'s correlation analysis.
SLC10A3 was upregulated in adrenocortical carcinoma, glioblastoma, and LGG and was associated with good overall survival (OS) in adrenocortical carcinoma and poor OS in LGG and glioblastoma. SLC10A3 was increased with increased World Health Organization grade, upregulated in isocitrate dehydrogenase-wild type, 1p/19q (chromosome arms 1p and 19q) non-co-deleted, and higher in astrocytoma. Patients with LGG were grouped by the occurrence of the clinical outcome endpoints (i.e., OS, disease-specific survival [DSS], and progression-free interval events). Genetic alterations in SLC10A3 were associated with poor progression-free survival in LGG. Most of clinical characteristics were associated with the SLC10A3 expression level. SLC10A3 with diagnostic and prognostic value (OS, DSS, and progression-free interval) was an independent prognostic factor in LGG. Moreover, Nomograms (WHO grade, 1p/19q codeletion, age and SLC10A3) had moderately accurate predictive for OS and DSS. Functional analysis showed that SLC10A3 might participate in the transport of multiple substances, neurogenic signaling, immune response, and programmed cell death in LGG. SLC10A3 correlated with immune infiltration in LGG and moderately correlated with the gene signature of pyroptosis, lysosome-dependent cell death, necroptosis, apoptosis, ferroptosis, alkaliptosis, and autophagy-dependent cell death.
SLC10A3 is a potential diagnostic and prognostic biomarker for LGG and might be associated with substance transport, neurogenic signaling, immune infiltration, and programmed cell death in LGG.
摘要：
背景：SLC10A3与低级别胶质瘤（LGG）之间的关联尚不清楚。
方法：我们使用公共数据库和生物信息学分析来分析SLC10A3，包括TCGA，GTEx,CGGA,HPA,GeneCards,cBioPortal,STRING,GEPIA2,TIMER,TISIB,接收机工作特性(ROC)曲线,Kaplan-Meier分析,Cox分析,列线图,校准图,GO/KEGG富集分析，基因集富集分析(GSEA)，单样本基因集富集分析(ssGSEA)，斯皮尔曼相关分析。
结果：SLC10A3在ACC中上调，GBM和LGG，并与ACC中的良好操作系统相关联，LGG和GBM中的操作系统很差。SLC10A3随WHO等级增加,并在IDH-Mut中上调，1p/19q非共同删除，在星形细胞瘤中更高，具有临床结局终点的患者发生(OS，DSS和PFI事件)在LGG中。SLC10A3的遗传改变与LGG较差的PFS有关。大多数临床特征与SLC10A3的表达水平相关。具有诊断和预后功能的SLC10A3(OS，DSS和PFI）值是LGG的独立预后因素，此外,SLC10A3对OS和DSS具有中等准确的预测性能。功能分析显示SLC10A3可能参与多种物质的转运,神经源性信号，LGG中的免疫反应和程序性细胞死亡。SLC10A3与LGG中的免疫浸润相关，与焦亡的基因签名中度相关，溶酶体依赖性细胞死亡,坏死,凋亡，铁性凋亡,细胞凋亡和自噬依赖性细胞死亡。
结论：SLC10A3是LGG的潜在诊断和预后生物标志物，并可能与物质运输有关，神经源性信号，LGG中的免疫浸润和程序性细胞死亡。
方法：我们使用公共数据库和生物信息学分析来分析SLC10A3，包括TCGA，GTEx,CGGA,HPA,GeneCards,cBioPortal,STRING,GEPIA2,TIMER,TISIB,接收机工作特性(ROC)曲线,Kaplan-Meier分析,Cox分析,列线图,校准图,GO/KEGG富集分析，基因集富集分析(GSEA)，单样本基因集富集分析(ssGSEA)，斯皮尔曼相关分析。
结果：SLC10A3在ACC中上调，GBM和LGG，并与ACC中的良好操作系统相关联，LGG和GBM中的操作系统很差。SLC10A3随WHO等级增加,并在IDH-Mut中上调，1p/19q非共同删除，在星形细胞瘤中更高，具有临床结局终点的患者发生(OS，DSS和PFI事件)在LGG中。SLC10A3的遗传改变与LGG较差的PFS有关。大多数临床特征与SLC10A3的表达水平相关。具有诊断和预后功能的SLC10A3(OS，DSS和PFI）值是LGG的独立预后因素，此外,SLC10A3对OS和DSS具有中等准确的预测性能。功能分析显示SLC10A3可能参与多种物质的转运,神经源性信号，LGG中的免疫反应和程序性细胞死亡。SLC10A3与LGG中的免疫浸润相关，与焦亡的基因签名中度相关，溶酶体依赖性细胞死亡,坏死,凋亡，铁性凋亡,细胞凋亡和自噬依赖性细胞死亡。
结论：SLC10A3是LGG的潜在诊断和预后生物标志物，并可能与物质运输有关，神经源性信号，LGG中的免疫浸润和程序性细胞死亡。
