Identification of Core Genes and Potential Drugs for Castration-Resistant Prostate Cancer Based on Bioinformatics Analysis.

Abstract

Prostate cancer (PCa) is a common malignant tumor in elderly men worldwide. Most primary PCas inevitably progress into castration-resistant prostate cancer (CRPC) after androgen deprivation therapy. The mechanisms contributing to this progression are still controversial. In this study, functional module genes, DNA methylations, core regulators, and potential drugs in primary PCa and CRPC were explored by integrating a series of bioinformatics analyses. First, 588 differentially expressed genes (DEGs) were identified. Combined with related genes, protein-protein interaction networks were constructed, and 22 and 14 significant modules were identified in primary PCa and CRPC, respectively. More DEGs were identified in differentially methylated genes in CRPC modules. The hub genes in CRPC included CDC20 and CDK1. Moreover, core noncoding RNAs and transcription factors that significantly regulate CRPC modules were identified, including TUG1, MALAT1, E2F3, and MED1. Finally, the prediction of potential drugs for primary PCa and CRPC was also performed. Exisulind and phosphodiesterase-4 inhibitors were predicted as potential drugs for CRPC. The results of this study provide a new way for biologists and pharmacists to understand the potential molecular mechanisms of CRPC and also provide valuable references for drug redirection and new drug development for PCa.