Identification of The Potential Signature Genes Between Lung Adenocarcinoma and Lung Squamous Cell Carcinoma

Abstract

Objectives:The purpose of this study was to identify and compare the potential signature genes along with the key pathways related to the pathogenesis of lung adenocarcinoma and lung squamous cell carcinoma through bioinformatics analysis.Methods:The differential expressions of miRNAs (DEmiRNAs) and mRNAs (DEmRNAs) in lung adenocarcinoma (AD) and lung squamous cell carcinoma (SC) were identified using the microarray data of 2miRNA and 6 mRNA from the Gene Expression Omnibus (GEO) database. The interaction between the DEmiRNAs and DEmRNAs was explored, followed by the KEGG pathway enrichment, Gene Ontology annotation (GO) enrichment analysis, DEmiRNA-gene interactive network, and protein-protein interaction (PPI) network to predict the hub genes and identify the key pathways. The sequencing data was then downloaded from The Cancer Genome Atlas (TCGA) to validate the hub genes, perform survival analysis, construct the ROC curve along with identifying the regulatory networks of mRNA-miRNA-lncRNA. Finally, the resulting signature genes and significant regulatory networks in AD and SC were filtrated across these analyses.Results:The DEmiRNAs and DEmRNAs were found to be significantly enriched in the phagosomes, human T-cell leukemia virus 1 infection, and ECM-receptor interaction in the AD, whereas in SC, they were enriched in the cell cycle and p53 signaling pathways. Furthermore, we found that the hsa-miR-21-5p, hsa-miR-200a-5p, and COL1A1 may act as potential meaningful biomarkers for the AD while hsa-miR-141-3p, hsa-miR-429, hsa-miR-130b-3p, hsa-miR-205-5p, and FRMD6 may play an important role in SC. The HMGA1/hsa-miR-424-5p/PVT1 maybe a significant regulatory network of AD while KIF11/hsa-miR-30d-5p/DLEU2, CCNE2/hsa-miR-30d-5p/DLEU2, and SPTBN1/hsa-miR-218-5p/MAGI2-AS3 may be the useful networks in regulating the SC progression.Conclusion: This study provided the signature targets and theoretical basis for further research on the biomarkers and molecular mechanisms of the SC, AD, and NSCLC.