应该制定激素相关治疗以外的策略来降低前列腺癌死亡率，以实现更好的疾病管理。在这里，我们表明 FUBP1 及其甲基化对于前列腺癌的进展至关重要，并且干扰 FUBP1 甲基化的竞争性肽可以抑制前列腺癌的发展。 FUBP1 在各种临床前模型中加速了前列腺癌的发展。 PRMT5 介导的 FUBP1 甲基化（受 BRD4 调节）对其致癌作用至关重要，并且与我们的患者队列中较早的生化复发和较短的治疗持续时间相关。在表达缺乏 PRMT5 介导的甲基化的 FUBP1 突变体的不同基因小鼠模型中观察到前列腺癌进展受到抑制。通过纳米复合物传递的竞争性肽，在不同的临床前模型中成功地破坏了 FUBP1 与 PRMT5 的相互作用，阻断了 FUBP1 甲基化，并抑制了前列腺癌的发展。总的来说，我们的研究结果表明，靶向 FUBP1 甲基化为疾病前列腺癌的管理提供了一种潜在的治疗策略。

Strategies beyond hormone-related therapy should need to be developed to improve prostate cancer mortalityfor better disease management. Here we show that FUBP1 and its methylation are essential for prostate cancer progression, and a competitive peptide interfering with FUBP1 methylation suppresses the development of prostate cancer. FUBP1 accelerated prostate cancer development across in various pre-clinical models. PRMT5-mediated FUBP1 methylation, regulated by BRD4, was crucial for its oncogenic effect and correlated with earlier biochemical recurrence shorter treatment durations in our patient cohort. Suppressed prostate cancer progression was observed in different various genetic mouse models expressing FUBP1 mutants deficient in PRMT5-mediated methylation. A competitive peptide, which was delivered through nanocomplexes, successfully disrupted the interaction of FUBP1 with PRMT5, blocked FUBP1 methylation, and inhibited prostate cancer development in different various pre-clinical models. Overall, our findings suggest that targeting FUBP1 methylation provides a potentially therapeutic strategy for disease prostate cancer management.