Objective: This study is to identify Small Cell Lung Cancer (SCLC) driver genes, annotate enrichment functions and key pathways, and also verify Monastrol therapeutic effect. Methods: The gene expression profiles of GSE40275 and GSE43346 was analyzed to identify the DEGs (Differentially Expressed Genes) between SCLC and the normal tissue. GO (Gene Ontology), KEGG (Kyoto Encyclopedia of Genes and Genomes) analysis and PPI (Protein-protein interaction) network analysis were conducted to find out the enrichment functions, pathways and hub genes. Moreover, in vitro, MTT assay, colony-forming assay, and the scratch assay were performed to verify the effect of Monastrol. Results: There were common 129 up-regulated and 176 down-regulated DEGs between SCLC samples and normal lung samples. KIF11, NDC80 and PBK were identified as hub genes after PPI network analysis. The q-PCR results showed that genes KIF11, NDC80 and PBK consistently expressed higher in cancer cells than normal cell lines. And in vitro assay showed that Monastrol inhibited SCLC cellular viability, proliferation and migration (P < 0.01). Conclusion: KIF11, NDC80 and PBK were aberrantly expressed and could be potentially applied as diagnostic biomarkers, therapeutic targets and prognostic biomarkers. Monastrol was a promising drug in treatment of SCLC patients. Key words: bioinformatics; lung science; SCLC; Monastrol.
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