Ren Zhishuai, Ma Shenqian, Cheng Xingbo, Guo Yuqi, Liu Zhendong
Zhengzhou University People's Hospital, Henan Provincial People's Hospital Zhengzhou 450003, Henan, China.
Department of Neurosurgery, The First Affiliated Hospital of Harbin Medical University Harbin 150001, Heilongjiang, China.
Int J Clin Exp Pathol. 2021 Sep 15;14(9):938-955. eCollection 2021.
In recent years, studies have shown that , as an oncogene, is involved in progression of cancers. However, its relationship with prognosis in glioma patients is rarely reported. Our purpose was to explore the role of in glioma. Based on 1814 glioma samples from multiple databases such as The Cancer Genome Atlas (TCGA), The Chinese Glioma Genome Atlas (CGGA), and The Gene Expression Omnibus (GEO), we use a variety of bioinformatics methods to verify the mechanism of action of in glioma from mRNA to protein, from appearance to mechanism analysis, from clinical features to prognosis. Then, the connectivity map (CMap) tool was used to predict drugs that inhibit the expression of . First, we found is highly expressed in glioma at mRNA and protein levels. Second, is an independent risk factor in prognosis and has suitable clinical diagnostic value in glioma. It was also positively correlated with World Health Organization (WHO) grade, age, and histology, and negatively correlated with mutation and codeletion. Third, base excision, cell cycle, and mismatch repair pathway were activated by in glioma. We predict small molecules to inhibit such as 8-azaguanine, gw8510, 6-thioguanosine, and ursodeoxycholic acid. This study is the first comprehensive analysis of , revealing a relationship between this novel oncogene, clinical characteristics of patients with glioma, and a mechanism leading to poor prognosis. It also provides a biomarker for diagnosis and treatment of glioma and reveal the pathologic progress of glioma at the genetic level.
近年来,研究表明,作为一种癌基因,其参与癌症进展。然而,它与胶质瘤患者预后的关系鲜有报道。我们的目的是探讨其在胶质瘤中的作用。基于来自癌症基因组图谱(TCGA)、中国胶质瘤基因组图谱(CGGA)和基因表达综合数据库(GEO)等多个数据库的1814例胶质瘤样本,我们运用多种生物信息学方法,从mRNA到蛋白质、从表象到机制分析、从临床特征到预后,全面验证其在胶质瘤中的作用机制。然后,使用连通性图谱(CMap)工具预测抑制其表达的药物。首先,我们发现其在胶质瘤中的mRNA和蛋白质水平均高表达。其次,它是预后的独立危险因素,在胶质瘤中具有一定的临床诊断价值。它还与世界卫生组织(WHO)分级、年龄和组织学呈正相关,与突变和缺失呈负相关。第三,在胶质瘤中通过激活碱基切除、细胞周期和错配修复途径发挥作用。我们预测8-氮杂鸟嘌呤、gw8510、6-硫代鸟嘌呤和熊去氧胆酸等小分子可抑制其表达。本研究首次对进行全面分析,揭示了这一新癌基因、胶质瘤患者临床特征以及导致预后不良机制之间的关系。它还为胶质瘤的诊断和治疗提供了生物标志物,并在基因水平揭示了胶质瘤的病理进展。