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• W2954432395 abstract "Abstract Lung adenocarcinomas injured greatly on the people worldwide. Although clinic experiments and gene profiling analyses had been well performed, to our knowledge, systemic coexpression analysis of human genes for this cancer is still limited to date. Here, using the published data GSE75037, we built the coexpression modules of genes by Weighted Gene Co‐Expression Network Analysis (WGCNA), and investigated function and protein–protein interaction network of coexpression genes by Database for Annotation, visualization, and Integrated Discovery (DAVID) and String database, respectively. First, 11 coexpression modules were conducted for 5,000 genes in the 83 samples recently. Number of genes for each module ranged from 90 to 1,260, with the mean of 454. Second, interaction relationships of hub‐genes between pairwise modules showed great differences, suggesting relatively high scale independence of the modules. Third, functional enrichment of the coexpression modules showed great differences. We found that genes in modules 8 significantly enriched in the biological process and/or pathways of cell adhesion, extracellular matrix (ECM)–receptor interaction, focal adhesion, and PI3K‐Akt signaling pathway, and so forth. It was inferred as the key module underlying lung adenocarcinomas. Furthermore, PPI analysis revealed that the genes COL1A1, COL1A2, COL3A1, CTGF , and BGN owned the largest number of adjacency genes, unveiling that they may functioned importantly during the occurrence of lung adenocarcinomas. To summary, genes involved in cell adhesion, ECM–receptor interaction, focal adhesion, and PI3K‐Akt signaling pathway play crucial roles in human lung adenocarcinomas." @default.
• W2954432395 created "2019-07-12" @default.
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• W2954432395 date "2019-07-01" @default.
• W2954432395 modified "2023-10-16" @default.
• W2954432395 title "Gene coexpression analysis offers important modules and pathway of human lung adenocarcinomas" @default.
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• W2954432395 doi "https://doi.org/10.1002/jcp.28985" @default.
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