OBJECTIVE: We aim to explore the expression difference between lung cancer cells and normal lung cells, and to investigate the mechanism of lung cancer development. Besides, we predicted the potential target site of transcriptional factors and microRNAs for differentially expressed genes (DEGs), which may help to regulate expression of DEGs. Small molecules were also identified to cure lung cancer. MATERIALS AND METHODS: Gene expression profiles we used were downloaded from Gene Expression Omnibus (GEO) using accession number of GSE2378. Firstly, we identified differential genes between lung cancer cells and normal lung cells by using R package limma. Then, we detected the processes and pathways that changed in lung cancer cells by Gene Ontology (GO) and KEGG pathway enrichment analysis. Potential target sites of transcriptional factors and microRNAs were also detected based on gene annotation data in MSigDB. Finally, small molecule drugs were screened via querying Connectivity Map database. RESULTS: We obtained 2961 differentially expressed genes between lung cancer cells and normal lung cells. Besides changes in cell cycle, metabolic processes and proteasome were also dramatically disordered. Some DEGs shared target sites of the transcription factor such as E2F, ETS and CEBPB. Target sites of hsa-miR-196a and hsa-miR-200c were also significantly enriched by DEGs. Iloprost simulated the state of normal cells, while MS-275 might be potential pathogenic substances. CONCLUSIONS: We investigate the lung cancer from Gene Ontology, pathway, transcription factors and microRNAs based on gene expression profiles. All these results may facilitate lung cancer treatment with a new breakthrough.
OBJECTIVE: We aim to explore the expression difference between lung cancer cells and normal lung cells, and to investigate the mechanism of lung cancer development. Besides, we predicted the potential target site of transcriptional factors and microRNAs for differentially expressed genes (DEGs), which may help to regulate expression of DEGs. Small molecules were also identified to cure lung cancer. MATERIALS AND METHODS: Gene expression profiles we used were downloaded from Gene Expression Omnibus (GEO) using accession number of GSE2378. Firstly, we identified differential genes between lung cancer cells and normal lung cells by using R package limma. Then, we detected the processes and pathways that changed in lung cancer cells by Gene Ontology (GO) and KEGG pathway enrichment analysis. Potential target sites of transcriptional factors and microRNAs were also detected based on gene annotation data in MSigDB. Finally, small molecule drugs were screened via querying Connectivity Map database. RESULTS: We obtained 2961 differentially expressed genes between lung cancer cells and normal lung cells. Besides changes in cell cycle, metabolic processes and proteasome were also dramatically disordered. Some DEGs shared target sites of the transcription factor such as E2F, ETS and CEBPB. Target sites of hsa-miR-196a and hsa-miR-200c were also significantly enriched by DEGs. Iloprost simulated the state of normal cells, while MS-275 might be potential pathogenic substances. CONCLUSIONS: We investigate the lung cancer from Gene Ontology, pathway, transcription factors and microRNAs based on gene expression profiles. All these results may facilitate lung cancer treatment with a new breakthrough.