Abstract

Prostate cancer (CaP) is a serious and common genital tumor. Generally, men with metastatic CaP can easily develop castration-resistant prostate cancer (CRPC). However, the pathogenesis and tumorigenic pathways of CRPC remain to be elucidated. The present study performed a comprehensive analysis on the gene expression profile of CRPC in order to determine the pathogenesis and tumorigenic of CRPC. The GSE33316 microarray, which consisted of 5 non-castrated samples and 5 castrated samples, was downloaded from the gene expression omnibus database. Subsequently, 201 upregulated and 161 downregulated differentially expressed genes (DEGs) were identified using the limma package in R and those genes were classified and annotated by plugin Mcode of Cytoscape. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using Database for Annotation, Visualization and Integrated Discovery and KEGG Orthology Based Annotation System 2.0 online tools to investigate the function of different gene modules. The BiNGO tool was used to visualize the level of enriched GO terms. Protein-protein interaction network was constructed using STRING and analyzed with Cytoscape. In conclusion, the present study determined that aldo-keto reductase 3, cyclin B2, regulator of G protein signaling 2, nuclear factor of activated T-cells and protein kinase C a may have important roles in the development of CRPC.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call