Unveiling the m6A Methylation Regulator Links between Prostate Cancer and Periodontitis by Transcriptomic Analysis

Abstract

Objective. To identify the N6-methyladenosine (m6A) methylation regulator genes linking prostate adenocarcinoma (PRAD) and periodontitis (PD). Materials and Methods. PD and TCGA-PRAD GEO datasets were downloaded and analyzed through differential expression analysis to determine the differentially expressed genes (DEGs) deregulated in both conditions. Twenty-three m6A RNA methylation-related genes were downloaded in total. The m6A-related genes that overlapped between PRAD and PD were identified as crosstalk genes. Survival analysis was performed on these genes to determine their prognostic values in the overall survival outcomes of prostate cancer. The KEGG pathways were the most significantly enriched by m6A-related crosstalk genes. We also performed lasso regression analysis and univariate survival analysis to identify the most important m6A-related crosstalk genes, and a protein-protein interaction (PPI) network was built from these genes. Results. Twenty-three m6A methylation-related regulator genes were differentially expressed and deregulated in PRAD and PD. Among these, seven (i.e., ALKBH5, FMR1, IGFBP3, RBM15B, YTHDF1, YTHDF2, and ZC3H13) were identified as m6A-related cross-talk genes. Survival analysis showed that only the FMR1 gene was a prognostic indicator for PRAD. All other genes had no significant influence on the overall survival of patients with PRAD. Lasso regression analysis and univariate survival analysis identified four m6A-related cross-talk genes (i.e., ALKBH5, IGFBP3, RBM15B, and FMR1) that influenced risk levels. A PPI network was constructed from these genes, and 183 genes from this network were significantly enriched in pathogenic Escherichia coli infection, p53 signaling pathway, nucleocytoplasmic transport, and ubiquitin-mediated proteolysis. Conclusion. Seven m6A methylation-related genes (ALKBH5, FMR1, IGFBP3, RBM15B, YTHDF1, YTHDF2, and ZC3H13) were identified as cross-talk genes between prostate cancer and PD.