Background: The aim of this study was to investigate the important role of pathway crosstalk and pathway dysfunction in the high-metastasis process of lung cancer cells, by using the microarray expression profiles of lung cancer cells at different metastasis levels.
Methods: The gene expression profile GSE10096 was downloaded from the Gene Expression Omnibus database, including 4 nonmetastasis samples, 3 low-metastasis samples (M1) and 3 high-metastasis samples (M5) of lung cancer cells. After the conversion from probe level to expression values using Jetset, the data were identified by limma package in R language to screen differentially expressed genes (DEGs). The pathways of DEGs were further enriched by the Kyoto Encyclopedia of Genes and Genomes (KEGG). A protein-protein interaction (PPI) network of genes related to the core pathway (pathway in cancer) and its neighbor pathways was constructed. Based on the PPI network, significantly changed pathway crosstalk and pathways were analyzed.
Results: Compared with those in the M1 lung cancer cells, the pathways hsa00564 (glycerophospholipid metabolism) and hsa0098 (metabolism of xenobiotics by cytochrome P450) of the M5 lung cancer cells showed significant functional changes. The dysfunction of pathway crosstalk mainly occurred between pathways hsa0098 and hsa04916 (melanogenesis pathway) and other pathways.
Conclusions: The results of our analysis indicate the significance of pathway crosstalk dysfunction and pathway dysfunction of M1 and M5 lung cancer cells as shown by bioinformatics methods. The present findings have the potential to lead to the study of the mechanisms of lung cancer in future.