Identification of key genes and pathways in benign prostatic hyperplasia

• Published in: Journal of cellular physiology Vol. 234; no. 11; pp. 19942 - 19950
• Main Authors: Ke, Zhi‐Bin, Cai, Hai, Wu, Yu‐Peng, Lin, Yun‐Zhi, Li, Xiao‐Dong, Huang, Jin‐Bei, Sun, Xiong‐Lin, Zheng, Qing‐Shui, Xue, Xue‐Yi, Wei, Yong, Xu, Ning
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.11.2019
• Subjects: Adenosine triphosphate; Adhesion; AKT1 protein; Annotations; ATP; Autophagy; Benign; benign prostatic hyperplasia; Binding; bioinformatics analysis; Cyclin B1; Cytoplasm; Cytosol; Encyclopedias; Forkhead protein; Gene expression; Genes; Genital diseases; Genomes; Geriatrics; Golgi apparatus; Hyperplasia; key genes; Kinases; Membrane proteins; Mitochondria; Molecular modelling; Pathogenesis; pathways; Phagocytosis; Polo-like kinase 1; Prostate; Protein-serine/threonine kinase; Proteins; Signal transduction; Signaling; Ubiquitin; Urinary tract; pathways; key genes; bioinformatics analysis; benign prostatic hyperplasia
• ISSN: 0021-9541; 1097-4652; 1097-4652
• DOI: 10.1002/jcp.28592

Benign prostatic hyperplasia (BPH) is one of the most common causes of lower urinary tract symptoms (LUTS) in elderly man. However, the underlying molecular mechanisms of BPH have not been completely elucidated. We identified the key genes and pathways by using analysis of Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were identified using edgeR. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed for the DEGs by Database for Annotation, Visualization and Integrated Discovery (DAVID) database and ConsensusPathDB, respectively. Then, protein–protein interaction (PPI) networks were established by the Search Tool for the Retrieval of Interacting Genes (STRING) database and visualized by Cytoscape software. Finally, we identified 660 DEGs ultimately including 268 upregulated genes and 392 downregulated genes. GO analysis revealed that DEGs were mainly enriched in extracellular exosome, identical protein binding, mitochondrial adenosine triphosphate (ATP) synthesis coupled proton transport, extracelluar matrix, focal adhesion, cytosol, Golgi apparatus, cytoplasm, protein binding, and Golgi membrane. Focal adhesion pathway, FoxO signaling pathway, and autophagy pathway were selected. Ubiquitin‐conjugating enzyme E2 C (UBE2C), serine/threonine kinase (AKT1), mitogen‐activated protein kinase 1 (MAPK1), cyclin B1 (CCNB1), polo‐like kinase 1 (PLK1) were filtrated as the hub genes according to the degree of connectivity from the PPI network. The five hub genes including UBE2C, AKT1, MAPK1, CCNB1, PLK1 may play key roles in the pathogenesis of benign prostatic hyperplasia (BPH). Focal adhesion pathway, FoxO signaling pathway, and autophagy pathway may be crucial for the progression of BPH. Comprehensive bioinformatics methods were applied in our study to analyze the functional enrichment and pathways of the differentially expressed genes in benign prostatic hyperplasia (BPH). Focal adhesion pathway, FoxO signaling pathway, and autophagy pathway may be crucial for the progress of BPH. Ubiquitin‐conjugating enzyme E2 C (UBE2C), serine/threonine kinase (AKT1), mitogen‐activated protein kinase 1 (MAPK1), cyclin B1 (CCNB1), polo‐like kinase 1 (PLK1) may be the key genes that play important roles in BPH. These results might facilitate further insights into the underlying pathogenesis of BPH.