Portrait of Molecular Signaling and Putative Therapeutic Targets in Prostate Cancer with Fusion.

Gene fusion between androgen receptor (AR) response genes and E26 transformation-specific (ETS) family members increases the gene expression of ETS family members, and promotes tumorigenesis in prostate cancer. However, the molecular features of fusion in prostate cancer are not fully understood, and drugs targeting fusion have not been developed. To examine key cellular signaling pathways and explore therapeutic targets and drugs for -fusion-positive prostate cancer, we analyzed RNA sequencing data and clinical information for prostate cancer. The -fusion-positive group was selected through prior study and analysis comparing -fusion-positive and -negative groups was conducted using a Pearson correlation test. We obtained 393 genes correlated with expression. Pathway analysis was performed using over-representation analysis (ORA), and six cancer-specific molecular signaling pathways (the irinotecan pathway, metabolism, androgen receptor signaling, interferon signaling, MAPK/NF-kB signaling, and the tamoxifen pathway) were altered in the -fusion-positive group. Furthermore, a gene-drug database was used to find an actionable drug and therapeutic target for the -fusion-positive group. Here, we have identified significantly altered genes and oncogenic signaling pathways in -fusion-positive prostate cancer, and we suggest therapeutic targets and potential drugs for -fusion-positive prostate patients.