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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 <i>ETV4</i> fusion in prostate cancer are not fully understood, and drugs targeting <i>ETV4</i> fusion have not been developed. To examine key cellular signaling pathways and explore therapeutic targets and drugs for <i>ETV4</i>-fusion-positive prostate cancer, we analyzed RNA sequencing data and clinical information for prostate cancer. The <i>ETV4</i>-fusion-positive group was selected through prior study and analysis comparing <i>ETV4</i>-fusion-positive and -negative groups was conducted using a Pearson correlation test. We obtained 393 genes correlated with <i>ETV4</i> 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 <i>ETV4</i>-fusion-positive group. Furthermore, a gene–drug database was used to find an actionable drug and therapeutic target for the <i>ETV4</i>-fusion-positive group. Here, we have identified significantly altered genes and oncogenic signaling pathways in <i>ETV4</i>-fusion-positive prostate cancer, and we suggest therapeutic targets and potential drugs for <i>ETV4</i>-fusion-positive prostate patients.