Identification of Glioma Specific Genes as Diagnostic and Prognostic Markers for Glioma

被引:2
作者
Tu, Ming [1 ]
Ye, Ling [2 ]
Hu, ShaoBo [1 ]
Wang, Wei [3 ]
Zhu, Penglei [4 ]
Lu, XiangHe [1 ]
Zheng, WeiMing [1 ]
机构
[1] Wenzhou Med Univ, Affiliated Hosp 1, Dept Neurosurg, Wenzhou, Zhejiang, Peoples R China
[2] Jinan Univ, Affiliated Hosp 1, Oncol Dept, Guangzhou, Guangdong, Peoples R China
[3] Wenzhou Med Univ, Affiliated Hosp 2, Dept Emergency, Wenzhou, Zhejiang, Peoples R China
[4] Wenzhou Peoples Hosp, Dept Neurosurg, Wenzhou, Zhejiang, Peoples R China
关键词
Glioma; glioma specific gene; biomarker; prediction; protein-protein interaction; prognosis; POOR-PROGNOSIS; EXPRESSION; PROLIFERATION; GNAO1;
D O I
10.2174/1574893615999200424090954
中图分类号
Q5 [生物化学];
学科分类号
071010 ; 081704 ;
摘要
Malignant gliomas are the most prevalent malignancy of the brain. However, there is still a lack of sensitive and accurate biomarkers for gliomas. In this study, we focused on exploring gliomas specific expressed genes as biomarkers. We evaluated whole-genome genes expression levels in 19 different types of human cancers by analyzing The Cancer Genome Atlas (TCGA) dataset. A total of 698 gliomas specific expressed genes were identified. A protein-protein interacting network was constructed to reveal the potential roles of these gliomas specific genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analysis showed that gliomas specific expressed genes were involved in regulating neuroactive ligand-receptor interaction, retrograde endocannabinoid signaling, Glutamatergic synapse, chemical synaptic transmission, nervous system development, central nervous system development, and learning. Of note, GRIA1, GNAO1, GRIN1, CACNA1A, CAMK2A, and SYP were identified to be downregulated and associated with poor prognosis in gliomas. The loss of function assay showed that GNAO1 knockdown significantly promoted U87 cell proliferation and cell cycle progression. We thought this study would provide novel biomarkers for gliomas.
引用
收藏
页码:120 / 129
页数:10
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