The progression of prostate cancer (PCa) relies on the activation of the androgen receptor (AR) by androgens. Despite efforts to block this pathway through androgen deprivation therapy, resistance can occur through several mechanisms, including the abnormal activation of AR, resulting in castration-resistant PCa following the introduction of treatment. Mutations, amplifications, and splicing variants in AR-related genes have garnered attention in this regard. Furthermore, recent large-scale next-generation sequencing analysis has revealed the critical roles of AR and AR-related genes, as well as the DNA repair, PI3K, and cell cycle pathways, in the onset and progression of PCa. Moreover, research on epigenomics and microRNA has increasingly become popular; however, it has not translated into the development of effective therapeutic strategies. Additionally, treatments targeting homologous recombination repair mutations and the PI3K/Akt pathway have been developed and are increasingly accessible, and multiple clinical trials have investigated the efficacy of immune checkpoint inhibitors. In this comprehensive review, we outline the status of PCa research in genomics and briefly explore potential future developments in the field of epigenetic modifications and microRNAs.
前列腺癌（PCa）的进展依赖于雄激素对雄激素受体（AR）的激活。尽管通过雄激素剥夺疗法阻断这一通路，但耐药仍可通过多种机制发生，包括AR的异常激活，导致治疗开始后出现去势抵抗性前列腺癌。AR相关基因的突变、扩增及剪接变异在此方面已引起关注。此外，近期大规模新一代测序分析揭示了AR及AR相关基因，以及DNA修复、PI3K和细胞周期通路在前列腺癌发生与进展中的关键作用。同时，表观基因组学与微小RNA的研究日益受到重视，但尚未转化为有效治疗策略的开发。此外，针对同源重组修复突变及PI3K/Akt通路的治疗方法已逐步发展并日益普及，多项临床试验已探讨了免疫检查点抑制剂的疗效。在本综述中，我们概述了前列腺癌基因组学的研究现状，并简要探讨了表观遗传修饰与微小RNA领域未来的潜在发展方向。
肿瘤(癌症)患者之家