Small cell lung cancer (SCLC) is one of the highly malignant tumors and a serious threat to human health. The aim of the present study was to explore the underlying molecular mechanisms of SCLC. mRNA microarray datasets GSE6044 and GSE11969 were downloaded from Gene Expression Omnibus database, and the differentially expressed genes (DEGs) between normal lung and SCLC samples were screened using GEO2R tool. Functional and pathway enrichment analyses were performed for common DEGs using the DAVID database, and the protein-protein interaction (PPI) network of common DEGs was constructed by the STRING database and visualized with Cytoscape software. In addition, the hub genes in the network and module analysis of the PPI network were performed using CentiScaPe and plugin Molecular Complex Detection. Finally, the mRNA expression levels of hub genes were validated in the Oncomine database. A total of 150 common DEGs with absolute fold-change >0.5, including 66 significantly downregulated DEGs and 84 upregulated DEGs were obtained. The Gene Ontology term enrichment analysis suggested that common upregulated DEGs were primarily enriched in biological processes (BPs), including ‘cell cycle’, ‘cell cycle phase’, ‘M phase’, ‘cell cycle process’ and ‘DNA metabolic process’. The common downregulated genes were significantly enriched in BPs, including ‘response to wounding’, ‘positive regulation of immune system process’, ‘immune response’, ‘acute inflammatory response’ and ‘inflammatory response’. Kyoto Encyclopedia of Genes and Genomes pathway analysis identified that the common downregulated DEGs were primarily enriched in the ‘complement and coagulation cascades’ signaling pathway; the common upregulated DEGs were mainly enriched in ‘cell cycle’, ‘DNA replication’, ‘oocyte meiosis’ and the ‘mismatch repair’ signaling pathways. From the PPI network, the top 10 hub genes in SCLC were selected, including topoisomerase IIα, proliferating cell nuclear antigen, replication factor C subunit 4, checkpoint kinase 1, thymidylate synthase, minichromosome maintenance protein (MCM) 2, cell division cycle (CDC) 20, cyclin dependent kinase inhibitor 3, MCM3 and CDC6, the mRNA levels of which are upregulated in Oncomine SCLC datasets with the exception of MCM2. Furthermore, the genes in the significant module were enriched in ‘cell cycle’, ‘DNA replication’ and ‘oocyte meiosis’ signaling pathways. Therefore, the present study can shed new light on the understanding of molecular mechanisms of SCLC and may provide molecular targets and diagnostic biomarkers for the treatment and early diagnosis of SCLC.

Brain metastasis from lung cancer (BMLC) is one of the common types of metastasis associated with poor prognosis. The aim of the present study was to elucidate the underlying molecular mechanisms of BMLC. The mRNA microarray dataset GSE18549 was downloaded from the Gene Expression Omnibus database. The Limma package of R was used to screen the differentially expressed genes (DEGs). Based on the DAVID database, functional and pathway enrichment analyses of DEGs were performed. Furthermore, the protein-protein interaction (PPI) network was predicted using the STRING database and visualized with Cytoscape software. In addition, hub genes and significant modules were selected based on the network. A total of 190 DEGs with log 2 |(fold change)|>1, including 129 significantly downregulated DEGs and 61 upregulated DEGs, were obtained. Gene Ontology functional enrichment analysis indicated that downregulated DEGs were mainly associated with ‘immune response’, ‘cell activation’ and ‘leukocyte activation’, while the upregulated DEGs were involved in ‘DNA repair’ and ‘viral process’. Kyoto Encyclopedia of Genes and Genomes pathway analysis indicated that the downregulated DEGs were mainly enriched in ‘chemokine signaling pathway’, whereas the upregulated DEGs were associated with ‘oocyte meiosis’. Based on the PPI network, 9 hub genes were selected, namely tumor necrosis factor, C-C motif chemokine ligand (CCL) 2, CD34, vascular cell adhesion molecule 1, CD48, CD27, CCL19, C-X-C motif chemokine receptor 6 and C-C motif chemokine receptor 2. The present study sheds light on the molecular mechanisms of BMLC and may provide molecular targets and diagnostic biomarkers for BMLC.