Diao Peng-Yu, Li Shao-Xun, Peng Jin, Yang Ji-Hu, Pan Yu-Chen, Xu Xiang-Ping, Tang Han, Hu Jin-Xian, Zhao Hua-Fu, Huang Guo-Dong
Department of Neurosurgery, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital Shenzhen, Guangdong Province, China.
The Affiliated Huaian No.1 Hospital of Nanjing Medical University, Huai'an First People's Hospital Huai'an, Jiangsu Province, China.
Int J Clin Exp Pathol. 2020 May 1;13(5):979-988. eCollection 2020.
EP300-interacting inhibitor of differentiation 3 (EID3) is a member of the IED family and has been associated with tumorigenesis and tumor development in different cancer types. However, the role of EID3 in glioblastoma multiforme (GBM) prognosis is not clear. Whole transcriptome sequencing data of 249 and 149 GBM patients were collected from the Chinese Glioma Genome Atlas (CGGA) and The Cancer Genome Atlas (TCGA) database respectively. The correlation between EID3 expression and overall survival (OS)/clinical pathologic features of GBM patients was investigated. Based on the Wilcoxon rank-sum test, EID3 expression in GBM tissues was significantly lower than in normal brain tissues (P < 0.001), and significantly higher than in LGG (low-grade glioma) (P < 0.001).There was a significant correlation between high EID3 expression with poor OS in CGGA (P = 0.049) and TCGA data (P = 0.024). Gene set enrichment analysis (GSEA) data analysis revealed a significant difference (FDR < 0.25, NOM -value < 0.05) in the enrichment of MSigDB Collection (h.all.v6.2.symbols.gmt). A total of eight enriched pathways were identified in the high EID3 expression group, including Myc Targets V1, Kras signaling DN, and DNA repair pathways. Multivariate Cox regression analysis indicated that high expression of EID3 correlated with poor OS (P = 0.032, HR = 1.41, CI: 1.03-1.90). We conclude that EID3 could serve as an independent factor for predicting the prognosis of patients with GBM. Moreover, it is associated with GBM development through the regulation of the Myc Targets, Kras signaling DN, and DNA repair pathways.
EP300相互作用的分化抑制因子3(EID3)是IED家族的成员,并且与不同癌症类型的肿瘤发生和肿瘤发展相关。然而,EID3在多形性胶质母细胞瘤(GBM)预后中的作用尚不清楚。分别从中国胶质瘤基因组图谱(CGGA)和癌症基因组图谱(TCGA)数据库收集了249例和149例GBM患者的全转录组测序数据。研究了EID3表达与GBM患者总生存期(OS)/临床病理特征之间的相关性。基于Wilcoxon秩和检验,GBM组织中EID3的表达明显低于正常脑组织(P<0.001),且明显高于低级别胶质瘤(LGG)(P<0.001)。在CGGA(P = 0.049)和TCGA数据(P = 0.024)中,EID3高表达与较差的OS之间存在显著相关性。基因集富集分析(GSEA)数据分析显示,MSigDB Collection(h.all.v6.2.symbols.gmt)的富集存在显著差异(FDR<0.25,NOM值<0.05)。在EID3高表达组中总共鉴定出8条富集途径,包括Myc靶标V1、Kras信号转导DN和DNA修复途径。多变量Cox回归分析表明,EID3高表达与较差的OS相关(P = 0.032,HR = 1.41,CI:1.03 - 1.90)。我们得出结论,EID3可作为预测GBM患者预后的独立因素。此外,它通过调节Myc靶标、Kras信号转导DN和DNA修复途径与GBM的发展相关。