Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8644822 | Gene | 2018 | 32 Pages |
Abstract
According to our meta-analyses, 830 and 1286 genes were differentially expressed in the TKIs-resistant EGFR-mutant NSCLC cell lines compared to TKIs-sensitive EGFR-mutant NSCLC cell lines in the absence and presence of TKIs treatment, respectively. PPI network analysis identified ESR1 and ELAVL1 to be the most highly ranked hub genes involved in the NSCLC acquired TKI-resistance. Moreover, gene set enrichment analyses indicated that up-regulated genes are mainly distributed in hallmarks “Glycolysis”, some “E2F targets”. Down-regulated genes mainly contribute to hallmarks “interferon alpha response”, “interferon gamma response”, and also “E2F targets”. For the first time, this study has demonstrated several robust candidate genes and pathways of the NSCLC acquired TKI-resistance. Further experimental verifications are highly recommended to examine our findings.
Keywords
GEOTKIsIMExGSEAREMDEGsEGFRVSNPPIMsigDBnESNCBIFDRPCAErlotinibEffect sizeGene Set Enrichment AnalysisPrincipal component analysisProtein-protein interactionGefitinibNSCLCNon-small cell lung cancerrandom effect modelNational Center for Biotechnology InformationTyrosine kinase inhibitorsfalse discovery ratenormalized enrichment scoreGene Expression OmnibusDifferentially expressed genesEpidermal growth factor receptor
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Authors
Marjan Mojtabavi Naeini, Manoochehr Tavassoli, Kamran Ghaedi,