前列腺癌（PRAD）是一种预后不良的高度恶性疾病，其发展受到复杂的基因和信号通路网络的调控。 LncRNA 和 miRNA 通过 ceRNA 网络在 PRAD 中发挥重要的调节作用。铜中毒是一种独特的程序性细胞死亡形式，涉及与肿瘤发展相关的各种信号通路和生物过程。激活 T 细胞核因子 5 (NFAT5) 是一种激活 T 细胞的转录因子，与铜凋亡有关。然而，NFAT5参与PRAD中ceRNA网络的调节机制仍不清楚。通过生物信息学分析，我们发现了调节铜凋亡的ceRNA轴。通过ROS测定和铜离子浓度测定，我们证明抑制NFAT5可以增加PRAD对铜凋亡诱导剂的敏感性。通过荧光素酶检测，我们发现AP000842.3作为miR-206的ceRNA来调节NFAT5的表达。在本研究中，我们发现lncRNA AP000842.3作为miR-206的ceRNA，参与了NFAT5的表达。 PRAD 中与铜凋亡相关的转录因子 NFAT5 水平的调节。首先，敲除NFAT5可以增加PRAD对铜凋亡诱导剂的敏感性。同时，AP000842.3和miR-206表达的变化可以通过调节NFAT5影响PRAD的增殖。从机制上讲，AP000842.3作为miR-206的ceRNA来调节NFAT5的表达。此外，lncRNA AP000842.3对PRAD和NFAT5恶性进展的影响部分依赖于miR-206。综上所述，我们的研究揭示了PRAD中关键的ceRNA调控网络，可被视为PRAD诊断的新的潜在靶点和治疗。

Prostate cancer (PRAD) is a highly malignant disease with poor prognosis, and its development is regulated by a complex network of genes and signaling pathways. LncRNAs and miRNAs have significant regulatory roles in PRAD through the ceRNA network. Cuproptosis is a unique form of programmed cell death that is involved in various signaling pathways and biological processes related to tumor development. Nuclear factor of activated T cells 5 (NFAT5), a transcription factor that activates T cells, has been implicated in cuproptosis. However, the regulatory mechanism by which NFAT5 is involved in the ceRNA network in PRAD remains unclear.Through bioinformatics analysis, we found the ceRNA axis that regulates cuproptosis. By performing ROS assay and copper ion concentration assay, we demonstrated that inhibiting NFAT5 can increase the sensitivity of PRAD to cuproptosis inducers. By using luciferase assay, we discovered that AP000842.3 acts as the ceRNA of miR-206 to regulate the expression of NFAT5.In this study, we found that lncRNA AP000842.3, as a ceRNA of miR-206, was involved in the regulation of levels of the transcription factor NFAT5 associated with cuproptosis in PRAD. First, knocking down NFAT5 can increase the sensitivity of PRAD to cuproptosis inducers. Meanwhile, changes in the expression of AP000842.3 and miR-206 could affect the proliferation of PRAD by regulating NFAT5. Mechanistically, AP000842.3 acts as the ceRNA of miR-206 to regulate the expression of NFAT5. In addition, the effects of lncRNA AP000842.3 on malignant progression of PRAD and NFAT5 were partially dependent on miR-206.Taken together, our study reveals a key ceRNA regulatory network in PRAD and can be regarded as a new potential target for PRAD diagnosis and treatment.