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Orai2 related transcriptome profile and clinical outcome in classical and mesenchymal subtype of glioblastoma

Feng Yuan  Li Yi  Long Hai  Tao Li  Luqing Tong  Yingshuai Wang  Haiwen Ma  Yihan Yang  Peidong Liu  Yang Xie  Jiabo Li  Yuheng Liu  Xuya Wang  Shengping Yu  Xuejun Yang  
【摘要】:Background Ca~(2+) release-activated Ca~(2+) channels(CRAC) is the main Ca~(2+) entry pathway regulating intracellular Ca~(2+) concentration in a variety of cancer types. Orai2 is the main pore-forming subunit of CRAC channels in central neurons. To characterize the role of Orai2 in gliomas, we investigated the biological process related, molecular function of Orai2 and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathways at transcriptome level and its clinical prognostic value.Methods Through The Cancer Genome Atlas(TCGA), French, Sun and Gene Expression Omnibus(GEO)(GSE23806) datasets, we systematically reviewed a total of 1231 cases with RNA-seq data and analyzed the functional annotation of Orai2 by Gene Ontology(GO) and KEGG pathway analysis. Univariate and multivariate survival analysis were performed in 823 patients with survival data. Results We found Orai2 was significantly upregulated in glioblastoma(GBM). Survival analysis suggested that higher-expression of Orai2 was independently associated with the worse prognosis of patients with classical and mesenchymal subtype of GBMs. According to TCGA transcriptional classification scheme, Orai2 expression was higher in tumors of classical and mesenchymal subtype than other subtypes, and shown significantly correlation with classical and mesenchymal related genes. GO and KEGG pathway analysis revealed that genes significantly correlated with Orai2 were involved in JNK signaling pathway. Through screening transcriptomic data, we found a strong connection between Orai2 and apoptosis, stemness and EMT-related genes(including Nestin, SOX2, NOTCH1, P53, Caspase 3, Cytochrome C, CDH2, ZEB1 and VIM). Conclusion Orai2 is a prognostic factor that is distinctly activated in the classical and mesenchymal subtype of GBM and that promotes glioma stem cells(GSCs) self-renewal, apoptosis process and mesenchymal transition via the JNK pathway. These findings suggested Orai2 as a candidate of therapeutic target for classical and mesenchymal subtype of GBM.

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