Several observational studies indicated a close association between prostate cancer and COVID-19. Nevertheless, whether there was a causal effect between them remained obscure. In this study, we aimed to detect the potential association between genetically determined prostate cancer and the risk of COVID-19. A bidirectional Mendelian randomization (MR) study was conducted to investigate the causal links between prostate cancer and COVID-19. Inverse variance weighted (IVW), MR-Egger, weighted median, weighted mode, and simple mode were used to estimate the causality. PIVW < 0.05 was considered statistically significant. The top single nucleotide polymorphisms associated with prostate cancer cases (n = 79,148) and COVID-19 cases (n = 54,071) were extracted from the summary genome-wide association study data obtained from a publicly available database. Cochran Q test was utilized to calculate the degree of heterogeneity. Additionally, we validated our findings in another replication cohort. In the forward MR study, the IVW method suggested no evidence for the causal effect of prostate cancer on COVID-19 susceptibility (OR = 1.00, 95%CI: 0.98-1.02, P = .978), COVID-19 hospitalization (OR = 1.05, 95%CI: 0.99-1.09, P = .054), and COVID-19 severity (OR = 1.03, 95%CI: 0.95-1.11, P = .453). Reverse MR analysis also showed no causal effect of COVID-19 diverse phenotypes on prostate cancer. Furthermore, the result of the East Asian cohort study was consistent with the European cohort. Sensitivity analysis showed no evidence of pleiotropy and heterogeneity. We did not discover genetic evidence to substantiate causal links between prostate cancer and COVID-19. Large-scale randomized controlled trials were required to enhance a more profound comprehension of this relationship in the future.