Abstract
BackgroundGlioma is one of the most common primary malignancies in the brain or spine. The transcription factor (TF) CCAAT/enhancer binding protein beta (CEBPB) is important for maintaining the tumor initiating capacity and invasion ability. To investigate the regulation mechanism of CEBPB in glioma, microarray data GSE47352 was analyzed.MethodsGSE47352 was downloaded from Gene Expression Omnibus, including three samples of SNB19 human glioma cells transduced with non-target control small hairpin RNA (shRNA) lentiviral vectors for 72 h (normal glioma cells) and three samples of SNB19 human glioma cells transduced with CEBPB shRNA lentiviral vectors for 72 h (CEBPB-silenced glioma cells). The differentially expressed genes (DEGs) were screened using limma package and then annotated. Afterwards, the Database for Annotation, Visualization, and Integrated Discovery (DAVID) software was applied to perform enrichment analysis for the DEGs. Furthermore, the protein-protein interaction (PPI) network and transcriptional regulatory network were constructed using Cytoscape software.ResultsTotal 529 DEGs were identified in the normal glioma cells compared with the CEBPB-silenced glioma cells, including 336 up-regulated and 193 down-regulated genes. The significantly enriched pathways included chemokine signaling pathway (which involved CCL2), focal adhesion (which involved THBS1 and THBS2), TGF-beta signaling pathway (which involved THBS1, THBS2, SMAD5, and SMAD6) and chronic myeloid leukemia (which involved TGFBR2 and CCND1). In the PPI network, CCND1 (degree = 29) and CCL2 (degree = 12) were hub nodes. Additionally, CEBPB and TCF12 might function in glioma through targeting others (CEBPB → TCF12, CEBPB → TGFBR2, and TCF12 → TGFBR2).Conclusions CEBPB might act in glioma by regulating CCL2, CCND1, THBS1, THBS2, SMAD5, SMAD6, TGFBR2, and TCF12.
Highlights
Glioma is one of the most common primary malignancies in the brain or spine
Du et al World Journal of Surgical Oncology (2016) 14:258 factor (TF) CCAAT/enhancer binding protein beta (CEBPB) is associated with the mesenchymal state of primary glioblastoma, and its expression in glioma is important for maintaining the tumor initiating capacity and invasion ability [9, 10]
A total of 74 samples were included in the dataset, among which 3 samples of SNB19 human glioma cells transduced with non-target control small hairpin RNA (shRNA) lentiviral vectors for 72 h and 3 samples of SNB19 human glioma cells transduced with CEBPB shRNA lentiviral vectors for 72 h (CEBPBsilenced glioma cells) were used to study the effect of CEBPB on glioma
Summary
Glioma is one of the most common primary malignancies in the brain or spine. The transcription factor (TF) CCAAT/enhancer binding protein beta (CEBPB) is important for maintaining the tumor initiating capacity and invasion ability. Glioma, which is known as one of the most common primary malignancies in the brain or spine, accounts for nearly 30 % of all brain and central nervous system tumors and 80 % of all malignant brain tumors [1, 2]. Previous researches have shown that the most important hallmarks of malignant glioma are its invasion and angiogenesis [3]. Du et al World Journal of Surgical Oncology (2016) 14:258 factor (TF) CCAAT/enhancer binding protein beta (CEBPB) is associated with the mesenchymal state of primary glioblastoma, and its expression in glioma is important for maintaining the tumor initiating capacity and invasion ability [9, 10]. The regulation mechanism of CEBPB on TGFB1/ SMAD3 in glioma was seldom studied
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