Posted: Tuesday, August 30, 2022
According to Gang Wu, PhD, of Tongji Hospital, Tongji University, Shanghai, China, and colleagues, primary prostate cancer eventually progresses to castration-resistant cancer after a period of androgen-deprivation therapy. Consequently, these investigators conducted a bioinformatic analysis to identify potential genes related to the development of enzalutamide-resistant, castration-resistant prostate cancer. Their results, which were published in the European Journal of Medical Research, focus on overexpression of CDK6.
“CDK6, a hub gene, plays an important role in the occurrence of prostate cancer and enzalutamide-resistant, castration-resistant prostate cancer,” the study authors mentioned. “Three small molecules, namely apigenin, chrysin, and fisetin, can decrease CDK6 expression and suppress enzalutamide-resistant prostate cancer cell proliferation. Therefore, they can be explored as potential drugs in treating enzalutamide-resistant, castration-resistant prostate cancer in the future.”
RNA-sequencing data on the enzalutamide-resistant, castration-resistant prostate cancer cell line LNCap were collected from GSE44905, GSE78201, and GSE150807 data sets of the Gene Expression Omnibus database. The expression profiles of the identified genes were verified, and the function of the potential drugs that may affect these genes was also evaluated.
A total of 43 upregulated and 2 downregulated differentially expressed genes were identified, along with 10 hub genes that appeared to correlate with the protein-protein interaction network. Of note, gene ontology enrichment results speculate that these differentially expressed genes were mainly active in the negative regulation of cell morphogenesis and differentiation.
Moreover, Kyoto Encyclopedia of Genes and Genome pathway enrichment analyses concluded that the enriched pathways were related to cytokine–cytokine receptor interaction and cancer development. Furthermore, CDK6 was found to be increased in all samples and cell lines of various prostate cancer subtypes. Accordingly, the suppression of CDK6 is predicted to delay the progress of prostate cancer.
Disclosure: The study authors reported no conflicts of interest.