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Background  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. To investigate the regulation mechanism of  CEBPB  in glioma, microarray data GSE47352 was analyzed.    Methods  GSE47352 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.    Results  Total 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 .

Microarray data analysis to identify crucial genes regulated by CEBPB in human SNB19 glioma cells