Network analysis in the identification of special mechanisms between small cell lung cancer and non-small cell lung cancer.

Abstract

To explore the similar and different pathogenesis between non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). This study used bioinformatics methods, including functional enrichment analysis, compared the topological features of SCLC and NSCLC in the human protein interaction network in a system aspect, and analyzed the highly intense modules from an integrated network. This study included 5082 and 2781 significantly different expression genes for NSCLC and SCLC, respectively. The differently expressed genes of NSCLC are mainly distributed in the extracellular region and synapse. By contrast, the genes of SCLC are located in the organelle, macromolecular complex, membrane-enclosed lumen, cell part, envelope, and synapse. Compared with SCLC, the differently expressed genes of NSCLC act in the biological regulation, multicellular organismal process, and viral reproduction and locomotion, which show that NSCLC is more likely to cause a wide range of cancer cell proliferation and virus infection than SCLC. The network topological properties of SCLC and NSCLC are similar, except the average shortest path length, which indicates that most of the genes of the two lung cancers play a similar function in the entire body. The commonly expressed genes show that all of the genes in the module may also cause NSCLC and SCLC, simultaneously. The proteins in module will involve the same or similar biological functions and the interactions among them induce the occurrence of lung cancer. Moreover, a potential biomarker of SCLC is the interaction between APIP and apoptotic protease activating factor (APAF)1, which share a common module.